Stem Cell Res Ther [JOURNAL]
Sun
200 papers
PBAE nanoparticle-mediated delivery of ASCL1 and NGN2 genes for astroglia-to-neuron reprogramming to remodel glial scar for spinal cord injury repair.
Guo J, Li L, Liu Z … +10 more , Yuan S, Ma X, Zhang D, Deng P, Wang J, Chen B, An J, Li J, Ma Q, Yang H
Stem Cell Res Ther · 2026 Jul · PMID 42401982 · Full text
BACKGROUND: Irreversible loss of neuronal cells elicited by neurotraumatic injuries or neurodegenerative disorders is particularly devastating due to the limited regenerative capacity of the central nervous system (CNS)....
BACKGROUND: Irreversible loss of neuronal cells elicited by neurotraumatic injuries or neurodegenerative disorders is particularly devastating due to the limited regenerative capacity of the central nervous system (CNS). Cell reprogramming-based therapies have emerged as promising therapeutic avenues for neuronal replenishment. However, their therapeutic potential in neural regeneration still faces formidable challenges, including risks of viral vector gene delivery, potential damage from cell transplantation, and significant glial scar (GS) formation following CNS injury. Therefore, developing an optimal approach that simultaneously replaces lost neurons and overcomes these persistent obstacles is crucial for neural regeneration and functional recovery. METHODS: We engineered a non-viral gene delivery platform using biodegradable poly(β-amino ester) (PBAE) nanoparticles (NPs) to effectively co-deliver plasmids encoding proneural transcription factors ASCL1 and NGN2 directly to astroglia (ATG) within GS region, in combination with neural induction. The biochemical and physiological properties of reprogrammed ATGs were characterized both in vivo and in vitro. The therapeutic potential of PBAE-A/N delivery was assessed in spinal cord injury (SCI) animal models through behavioral evaluations. Finally, the molecular mechanisms underlying ASCL1/NGN2-mediated ATG-to-neuron reprogramming were investigated. RESULTS: PBAE-mediated delivery of ASCL1/NGN2 plasmids effectively reprogrammed resident ATGs within GSs into functional neurons, as evidenced by the acquisition of neuronal morphology and biochemical phenotype (neuronal marker expression), loss of ATG characteristics, scar remodeling, and functionality indistinguishable from those of genuine neurons, including specialized calcium signaling, synaptic activity, and action potential firing. Critically, local administration of PBAE-ASCL1/NGN2 NPs into the GS region of the injured spinal cord significantly ameliorated neurological deficits. Mechanistically, this reprogramming event likely involved the modulation of downstream targeting signaling mediated by Cend1, RanBPM, and Dyrk1, along with crosstalk with the Notch1/Cyclin D1 axis. CONCLUSIONS: This study demonstrates that PBAE-mediated ASCL1/NGN2 delivery enables in situ reprogramming of ATG into functional neurons while actively dissolving GSs, thereby addressing both neuronal loss and GS barriers in CNS repair. The identified Cend1/RanBPM/Dyrk1 signaling and its crosstalk with Notch1/Cyclin D1 axis provide mechanistic insights into the events. Collectively, this work presents a novel therapeutic alternative for CNS repair and neurodegeneration by simultaneously replacing lost neurons and eliminating endogenous GSs through in situ cell reprogramming.
Lipoaspirate-derived secretome restores redox homeostasis to attenuate pathological scar formation.
Huang X, Ding P, Sun Z … +4 more , Xiang H, Wei M, Bi H, Zhao Z
Stem Cell Res Ther · 2026 Jul · PMID 42401927 · Full text
BACKGROUND: Pathological scars are characterized by persistent fibroblast activation and excessive extracellular matrix (ECM) deposition. Although oxidative stress and dysregulated NRF2 signaling contribute to TGF-β1-med...
BACKGROUND: Pathological scars are characterized by persistent fibroblast activation and excessive extracellular matrix (ECM) deposition. Although oxidative stress and dysregulated NRF2 signaling contribute to TGF-β1-mediated fibrosis in internal organs, their roles in cutaneous pathological scarring remain unclear. Secretome-based cell-free therapies have shown regenerative and antifibrotic potential, but whether lipoaspirate-derived secretome can restore fibroblast redox homeostasis and thereby attenuate pathological scarring is unknown. METHODS: Lipoaspirate fluid obtained during standard tumescent liposuction was processed by 100-kDa ultrafiltration to generate lipoaspirate-derived secretome (LA), while secretome from adipose-derived stromal cell (ADSC) culture supernatant served as a comparator (CS). LA and CS were characterized by nanoparticle tracking analysis, transmission electron microscopy, and immunoblotting for EV markers. In vivo efficacy was evaluated in a rabbit ear scar model with weekly intradermal LA injection, followed by gross, histological, collagen, and qPCR assessments. Comparative proteomic profiling of LA and CS was performed using data-independent acquisition LC-MS/MS with enrichment analysis, and paired human scar and normal skin samples were analyzed by single-cell RNA sequencing. In vitro, TGF-β1-stimulated fibroblasts were treated with LA or CS, and NRF2 involvement was assessed using the inhibitor ML385 or Nrf2-targeting siRNA. Redox balance, NRF2 signaling, and profibrotic responses were assessed by fluorometric assays, qPCR, and immunoblotting. RESULTS: LA showed a substantially higher particle yield than CS and contained abundant extracellular vesicles. Weekly intradermal LA injections reduced scar formation and improved collagen organization in the rabbit ear model. Comparative proteomics of LA versus CS highlighted cytoprotective pathways, including glutathione metabolism and NRF2-associated antioxidant signaling. Analyses of human scar tissues revealed elevated NOX4 expression, increased 4-HNE, and impaired NRF2-associated antioxidant signaling in scar fibroblasts. In vitro, both LA and CS attenuated TGF-β1-driven profibrotic fibroblast activation, whereas LA showed greater antioxidant activity, including stronger suppression of oxidative stress-related responses and improved GSH/GSSG balance. Pharmacological inhibition and genetic silencing of NRF2 partially reversed the antioxidant and antifibrotic effects of LA. CONCLUSION: Lipoaspirate-derived secretome (LA) is a clinically accessible cell-free therapeutic candidate for pathological scarring. LA restores redox homeostasis, in part through NRF2-associated antioxidant signaling, attenuates TGF-β1-driven profibrotic fibroblast activation, and improves scar remodeling in vivo. These findings support LA as a promising cell-free strategy for attenuating pathological scar formation.
Identification and enrichment of human retinal organoid-derived red/green cone-competent precursors with enhanced axon dynamics.
Susaimanickam PJ, Capowski E, Xiong MN … +11 more , Edwards KL, Phanse Y, Welch MJ, Pier A, Mayerl SJ, Zepeda MAF, Peterson KD, Phillips MJ, Sinha D, Gomez TM, Gamm DM
Stem Cell Res Ther · 2026 Jul · PMID 42401922 · Full text
BACKGROUND: Cell replacement therapies aimed at restoring foveal vision require a robust source of red/green (long/medium wavelength, or L/M) cone photoreceptors with intrinsic properties conducive to functional integrat...
BACKGROUND: Cell replacement therapies aimed at restoring foveal vision require a robust source of red/green (long/medium wavelength, or L/M) cone photoreceptors with intrinsic properties conducive to functional integration into host retina. Recent evidence has shown that cones present within mature human retinal organoids (ROs) can generate light responses comparable to macaque foveal cones. However, only cone precursors from early developing ROs possess a capacity for cell-autonomous axonogenesis. Therefore, we sought to identify and enrich for a population of early L/M cone-competent precursors with intrinsically superior axon dynamics that would provide an ideal donor cell source for future foveal reconstruction efforts. METHODS: We developed a dual L/M cone/rod reporter (L/M-CRR) line to unequivocally identify early L/M cone-competent precursors from human ROs. To do so, we used CRISPR/Cas9 to link a tdTomato transgene to the endogenous THRB2 promoter in the WA09 NRL rod reporter line. Differentiated ROs were characterized at early (day 50) and intermediate (day 100) developmental stages using a combination of live fluorescence imaging, immunocytochemistry, and flow cytometry, followed by fluorescence-activated cell sorting and bulk RNAseq analysis to delineate the unique molecular signature of early L/M cone-competent precursors. RESULTS: THRB2-driven tdTomato fluorescence faithfully demarcated L/M cone-competent precursors throughout RO development, although fluorescence declined in later ROs as L/M cones matured. Transcriptomic profiling revealed that day 50 sorted tdTomato cells were specifically enriched for genes associated with neural development, axon extension and guidance, and cell migration, which included a gene encoding the cell surface protein CD166/ALCAM. Magnetic-activated cell sorting using an anti-CD166 antibody resulted in specific enrichment of early, highly axonogenic L/M cone-competent precursors assessed by time-lapse imaging. CONCLUSIONS: The L/M-CRR line enables definitive identification and transcriptomic characterization of L/M cone-competent precursors throughout early to mid-stage RO development. Our investigation also revealed that CD166/ALCAM can be used to independently identify and enrich for a subset of early L/M cone-competent precursors that selectively display axon dynamicity conducive for retinal circuit integration. Our studies provide the first insights into early human L/M cone development and establish a method to isolate L/M cone-competent precursors with enhanced axon dynamics, which constitutes a compelling cell population for treating central vision loss caused by photoreceptor degeneration.
PTGIS inhibited osteogenic and promoted angiogenic differentiation of bone marrow mesenchymal stem cells via endoplasmic reticulum stress mediated PI3K/AKT signaling.
Bao H, Wang J, Yang H … +3 more , Liu H, Han X, Fan Z
Stem Cell Res Ther · 2026 Jul · PMID 42401884 · Full text
BACKGROUND: Mesenchymal stem cells (MSCs) play a key role in ectopic mineralization. Effective treatment requires both inhibiting pathological calcification and promoting vessel growth. While prostacyclin synthase (PTGIS...
BACKGROUND: Mesenchymal stem cells (MSCs) play a key role in ectopic mineralization. Effective treatment requires both inhibiting pathological calcification and promoting vessel growth. While prostacyclin synthase (PTGIS) is critical for vascular health, its role in regulating osteogenic and angiogenic differentiation in MSCs remains unclear. METHODS: Following PTGIS modulation in bone marrow mesenchymal stem cells (BMSCs), osteogenesis was assessed by alkaline phosphatase (ALP) activity, Alizarin Red staining (ARS), and hydroxyapatite/tricalcium phosphate (HA/TCP) particles implantation. Angiogenesis was evaluated via a co-culture system of BMSCs and human umbilical vein endothelial cells (HUVECs). Mechanistic studies involved Ca²⁺ dynamics, western blotting, and pharmacological inhibition. RESULTS: Knockdown of PTGIS enhanced ALP activity, mineralization, the expression of the osteogenic marker DMP1/BSP, and bone-like tissue formation both in vitro and in vivo. Conversely, PTGIS knockdown reduced tubule formation in vitro and impaired blood vessel formation, and the expression of the angiogenic marker CD31 in vivo. Mechanistically, the overexpression of PTGIS promoted Ca²⁺ efflux, endoplasmic reticulum (ER) dilation and vacuolization, increased the levels of the ER stress markers BIP/GRP75, and elevated PI3K/AKT phosphorylation. The inhibition of either ER stress or AKT activity restored osteogenic capacity by enhancing ALP activity and mineralization, and suppressed angiogenic capacity by inhibiting tubule formation in BMSCs. CONCLUSION: PTGIS inhibited osteogenic and promoted angiogenic differentiation of BMSCs through ER stress mediated PI3K/AKT signaling pathway. This PTGIS-dependent regulatory pathway offers new insight into MSC fate determination and represents a potential therapeutic strategy for treating ectopic mineralization disorders.
ITGA1 promotes osteogenic differentiation of human periodontal ligament stem cells via FAK-mediated PI3K-Akt activation.
Tan J, Tang H, Peng S … +9 more , Li X, Dai M, Xu M, Zhu S, Zhang R, Pi C, Jiang F, Yang K, Li J
Stem Cell Res Ther · 2026 Jul · PMID 42400080 · Full text
BACKGROUND: Human periodontal ligament stem cells (hPDLSCs) possess promising potential for bone regeneration; however, the regulation of their osteogenic differentiation remains incompletely understood. Integrin α1 (ITG...
BACKGROUND: Human periodontal ligament stem cells (hPDLSCs) possess promising potential for bone regeneration; however, the regulation of their osteogenic differentiation remains incompletely understood. Integrin α1 (ITGA1) has been implicated in multiple cellular processes, but its role in hPDLSC osteogenesis requires further investigation. METHODS: ITGA1 was overexpressed in hPDLSCs using an adenoviral vector, and osteogenic differentiation was evaluated by alkaline phosphatase (ALP) staining and gene expression analysis. Loss-of-function experiments were performed using ITGA1 knockdown. Data-independent acquisition (DIA) proteomics, protein-protein interaction (PPI) analysis, immunoprecipitation-mass spectrometry (IP-MS), and co-immunoprecipitation (Co-IP) were employed to explore the underlying mechanisms. Functional validation was performed using gene silencing and pharmacological inhibition, and in vivo efficacy was assessed in a rat mandibular bone defect model. RESULTS: Overexpression of ITGA1 enhanced osteogenic differentiation, while its knockdown produced the opposite effect. Proteomic analysis identified multiple differentially expressed proteins, including integrin family members, suggesting potential functional specificity. ITGA5 knockdown did not impair ITGA1-mediated osteogenesis. PPI and Co-IP analyses supported an interaction between ITGA1 and focal adhesion kinase (FAK). Inhibition of FAK or PI3K-Akt signalling reduced the pro-osteogenic effects of ITGA1. In vivo, transplantation of ITGA1-overexpressing hPDLSCs promoted bone regeneration in rat mandibular defects. CONCLUSIONS: Activation of the FAK/PI3K-Akt signalling pathway contributes to the promoting effect of ITGA1 on osteogenic differentiation of hPDLSCs. These findings provide insight into integrin-mediated regulation of hPDLSC osteogenesis and may inform future strategies for bone regeneration.
Therapeutic potential of mesenchymal stem cell-derived apoptotic vesicles in liver fibrosis: targeting the IGFBP3/PI3K-AKT axis via miR-409-3p.
Lu B, Chen X, Wang H … +10 more , Li M, Shi Y, Huang Y, Ding J, Wang Y, Li L, Luo J, Jia C, Lin N, Feng Y
Stem Cell Res Ther · 2026 Jul · PMID 42400044 · Full text
BACKGROUND: Hepatic fibrosis is a progressive pathology driven by hepatic stellate cell (HSC) activation and excessive extracellular matrix deposition. While mesenchymal stem cell (MSC) therapies show promise, their clin...
BACKGROUND: Hepatic fibrosis is a progressive pathology driven by hepatic stellate cell (HSC) activation and excessive extracellular matrix deposition. While mesenchymal stem cell (MSC) therapies show promise, their clinical translation is hindered by the inherent safety constraints of live cell transplantation. MSC-derived apoptotic vesicles (MSC-ApoVs), a structurally distinct class of extracellular vesicles, emerge as a compelling cell-free alternative. However, their specific therapeutic efficacy and mechanistic targets in hepatic fibrosis remain elusive. METHODS: MSC-ApoVs were isolated from human umbilical cord MSCs and stringently characterized to exclude non-vesicular contaminants. Their anti-fibrotic efficacy was evaluated in vitro using TGF-β1-activated LX-2 cells and in vivo within a CCl₄-induced murine fibrosis model. To elucidate and functionally validate the underlying mechanisms, we integrated transcriptomic profiling (RNA-seq), dual-luciferase reporter assays, and dual-directional pharmacological interventions. Furthermore, human clinical liver biopsies were analyzed to determine the clinico-pathological relevance of the identified targets. RESULTS: We demonstrated that MSC-ApoVs were efficiently internalized by HSCs, significantly blunting TGF-β1-induced activation, proliferation, and migration, alongside a marked reduction in fibrotic markers (α-SMA, MMP2, and Collagen-I). Transcriptomic screening identified Insulin-like Growth Factor Binding Protein 3 (IGFBP3) as a crucial pro-fibrotic mediator. Mechanistically, MSC-ApoV-enriched miR-409-3p directly targeted and downregulated IGFBP3, thereby restricting the PI3K-AKT signaling cascade-a dependency unequivocally validated by targeted rescue and blockade assays. In vivo, systemic MSC-ApoV administration robustly ameliorated CCl₄-induced hepatic fibrosis and restored liver function. Crucially, clinical analyses revealed a strong positive correlation between elevated IGFBP3 expression and the severity of human fibrotic progression. CONCLUSIONS: This study delineates a novel cell-free therapeutic paradigm, demonstrating that MSC-ApoVs mitigate hepatic fibrosis largely through the miR-409-3p-mediated silencing of the IGFBP3/PI3K-AKT axis. By integrating robust in vitro, in vivo, and clinical evidence, these findings highlight MSC-ApoVs as a highly efficacious and translatable alternative to traditional live stem cell therapies for hepatic fibrosis.
SERINC3 promotes osteogenic differentiation of BMSCs via IL-32/AMPK-mediated autophagy and mitochondrial energy metabolism.
Zheng Z, Xu T, Pathak JL … +10 more , Xu S, Lu J, Yu S, Fu Z, Xie W, Zhu H, Jaspers RT, Zheng H, Wu L, Li J
Stem Cell Res Ther · 2026 Jul · PMID 42400028 · Full text
BACKGROUND: SERINC3, a member of the serine incorporator protein family, is known for its roles in viral resistance and tumorigenesis, however, its function in osteogenesis remains unexplored. METHODS: Lentivirus infecti...
BACKGROUND: SERINC3, a member of the serine incorporator protein family, is known for its roles in viral resistance and tumorigenesis, however, its function in osteogenesis remains unexplored. METHODS: Lentivirus infection, alkaline Phosphatase/Alizarin Red S Staining, and RT-qPCR were used to evaluate the osteogenic differentiation of mesenchymal stem cells mediated by SERINC3. MicroCT, H&E, and Masson staining were performed to investigate the bone formation and bone defect repair via Serinc3 knockout (KO) mice and nude mice. RNA sequencing, Co-IP, Western blotting, and Seahorse energy metabolism analysis were performed to elucidate the regulatory mechanism of SERINC3. RESULTS: Here, we identify SERINC3 as a critical regulator of osteogenic differentiation of bone marrow-derived stem cells (BMSCs) and bone regeneration. SERINC3 expression was significantly upregulated during osteogenic differentiation of BMSCs and stem cells from human exfoliated deciduous teeth (SHED). Functional assays revealed that SERINC3 overexpression enhanced osteogenic differentiation, proliferation, and migration of MSCs, while Serinc3-KO impaired these processes and led to osteopenia in mice. In a calvarial defect model, Serinc3-KO mice exhibited 42% less bone volume (BV/TV) and 35% lower bone mineral density (BMD), whereas SERINC3-overexpressing BMSCs significantly improved bone repair. Mechanistically, RNA sequencing and pathway analysis revealed that SERINC3 interacts with IL32 to activate the AMPK-ULK1-autophagy axis, thereby promoting osteogenesis. Additionally, SERINC3 enhanced mitochondrial energy metabolism by upregulating tricarboxylic acid cycle enzymes (ACO1, DLAT, SDHA) and increasing oxygen consumption rates. Rescue experiments confirmed that AMPK inhibition or autophagy blockade abolished SERINC3-mediated osteogenic effects, whereas mitochondrial electron transport chain activators restored osteogenesis in SERINC3-knockdown cells. CONCLUSIONS: In summary, this study identifies SERINC3 as a novel regulator of bone formation that orchestrates osteogenesis through IL32-AMPK-autophagy signaling axis and mitochondrial metabolism. These findings highlight SERINC3 as a potential therapeutic target for enhancing bone regeneration and treating skeletal defects.
DLP bioprinting of cartilage organoid-laden bioinks yields high-fidelity auricular constructs with enhanced chondrogenesis.
Chen Y, Zhang Y, Luo P … +6 more , Su S, Jiang W, Luo C, Cai X, Sun J, Wang Z
Stem Cell Res Ther · 2026 Jul · PMID 42399996 · Full text
PURPOSE: To develop and validate a cartilage organoid (CO)-laden digital light processing (DLP) bioprinting strategy for auricular reconstruction and to compare its performance with conventional chondrocyte-laden prints....
PURPOSE: To develop and validate a cartilage organoid (CO)-laden digital light processing (DLP) bioprinting strategy for auricular reconstruction and to compare its performance with conventional chondrocyte-laden prints. MATERIALS AND METHODS: Rat bone-marrow stromal cells (BMSCs) were aggregated into spheroid and chondrogenically induced to form CO. Organoid construction and characterization included EdU proliferation assay, CD73/CD90 immunofluorescence (IF), and real-time quantitative polymerase chain reaction (qPCR) of chondrogenic genes. O-nitrobenzyl functionalized gelatin (GelNB)/ methacrylated hyaluronic acid (HAMA) bioinks were screened by gross morphology, tensile/ compressive mechanics, enzymatic degradability (0.1% collagenase II), and swelling, identifying 10% (w/v) GelNB + 1% (w/v) HAMA as the working bioink. Full-scale ears were DLP-printed from acellular, chondrocyte-laden, or CO-laden inks. In vitro, whole-mount Live/Dead imaging was performed at 7/14/21 days and qPCR quantified COL2A1, aggrecan (ACAN), COL10A1. In vivo, constructs were implanted subcutaneously in nude mice and analyzed at 4/8 weeks by Hematoxylin-eosin (H&E), Safranin O/Fast Green, ACAN and COL II IHC staining, and compressive Young's modulus measurement on implants. RESULTS: The 10% GelNB + 1% HAMA ink balanced print fidelity, mechanical robustness, and controlled degradability. Loading CO did not impair printability. During 21-day culture, viability remained high; at day 21, CO-laden ears showed higher COL2A1/ACAN and lower COL10A1 than chondrocyte-laden controls. After implantation, CO-laden explants exhibited more abundant lacuna-like cartilage morphology, stronger ACAN and COL II staining, increased EVG-positive elastic fiber-associated matrix, and a higher compressive Young's modulus at 8 weeks. CONCLUSIONS: CO-laden DLP bioprinting enhances chondrogenesis and mitigates hypertrophy versus chondrocyte-laden printing, offering an exploratory high-fidelity strategy for auricular cartilage-like tissue engineering rather than definitive mature elastic cartilage regeneration.
Adipose-derived stem cells-conditioned medium (ADMSCs-CM) improves testicular function and sperm DNA damage via Nrf2 antioxidant signaling pathways in rat unilateral varicocele.
Khosravi-Farsani S, Khadivi F, Rafiei M … +4 more , Ahmadi R, Khosravi-Farsani R, Amini-Khoei H, Rahmani F
Stem Cell Res Ther · 2026 Jul · PMID 42393810 · Full text
BACKGROUND: Varicocele is an excessive dilation of the pampiniform plexus. Although the accurate mechanism of varicocele-induced infertility is still unknown, oxidative stress plays a major function. A great attention ha...
BACKGROUND: Varicocele is an excessive dilation of the pampiniform plexus. Although the accurate mechanism of varicocele-induced infertility is still unknown, oxidative stress plays a major function. A great attention has recently been attracted towards the MSCs' secreted factors for the treatment of diseases. So, we investigated the effect of adipose derived stem cells-conditioned medium (ADMSCs- CM) on Nrf2 signaling pathway, downstream antioxidant enzymes, sperm DNA and acrosome damage following varicocele surgery. METHODS: Rats were divided into sham, varicocele, Varicocele + DMEM/F-12, and ADMSCs-CM groups. ADMSCs were isolated, confirmed, and ADMSCs-CM was prepared. Spermatogenesis quantification was done by H& E-stained testicular sections. The percentage of sperm DNA fragmentation and acrosome integrity was assessed through acridine orange and coomassie blue stainings. The testicular levels of MDA, TAC, SOD, and CAT were assessed. Relative expression of Nrf2/ Ho-1 genes evaluated through Real-time PCR. RESULTS: Mean percentage of sperm acrosome integrity, TDI, SPI, and Johnsen's criteria decreased (p < 0.0001), mean percentage of sperm DNA fragmentation (p < 0.0001), and testicular MDA (p < 0.001) significantly increased in the varicocele group. Unilateral varicocele reduced notably testicular levels of TAC (p < 0.0001), SOD (p < 0.01), and CAT (p < 0.05). ADMSCs-CM improved significantly sperm acrosome integrity (p < 0.01) and sperm DNA fragmentation (p < 0.05). Also, results demonstrated a remarkable recovery in spermatogenic parameters. There is a significant improvement in MDA, SOD (p < 0.05), and TAC (p < 0.01) levels in the ADMSCs-CM group. Treatment with AMSCs resulted in a non-significant increase in the mRNA expression of both Nrf2 and Ho-1 genes compared with the varicocele group, whereas a significant increase was observed compared with the sham group. CONCLUSIONS: Intratesticular administration of ADMSCs-CM could be a promising approach for the partial restoration of spermatogenesis and sperm damage potentially through Nrf2 antioxidant signaling pathway and reducing oxidative injury induced by varicocele.
PDLSC-CM targets HAPLN1 in macrophages to reduce root resorption in delayed replanted teeth.
Jia L, Zhao Z, Zhang Y … +12 more , Zhang L, Liu Y, Ma H, Zhang P, Liu X, Zhang L, Yang H, Yang Z, Ma Z, Wang H, Hou Z, Ma H
Stem Cell Res Ther · 2026 Jul · PMID 42393763 · Full text
BACKGROUND: Tooth avulsion is the most serious dental trauma, mainly affecting anterior teeth in adolescents. Delayed tooth replantation is the most common situation in clinical, but root resorption is a common complicat...
BACKGROUND: Tooth avulsion is the most serious dental trauma, mainly affecting anterior teeth in adolescents. Delayed tooth replantation is the most common situation in clinical, but root resorption is a common complication that can lead to tooth loss. As implant is not feasible in adolescents, strategies to mitigate root resorption remain a major challenge in dentistry. We aim to evaluate the therapeutic effect and potential target of periodontal ligament stem cell-conditioned medium (PDLSC-CM) to reduce root resorption in delayed replanted tooth. METHODS: Clinical samples from delayed tooth replantation patients were analyzed by X-ray and histological staining. A rat model of delayed tooth replantation was established, with PDLSC-CM applied as the tooth preservative and irrigating solution. Root resorption was assessed by micro-CT and histopathology. Proteomic screening followed by Western blot and immunofluorescence was used to identify and validate key molecules. Macrophage polarization and osteoclastogenesis were examined in vitro using RAW264.7 and bone marrow-derived macrophages. Recombinant adeno-associated virus (rAAV) was used to validate the key protein molecules. RESULTS: Human avulsed tooth with delayed replantation shows obvious root resorption and high expressions of inflammatory cytokines and osteoclast-related factors in periapical tissue. PDLSC-CM reduces the root resorption and inhibits the expressions of inflammatory cytokines and osteoclast-related factors in root and periapical tissue of delayed replantation of avulsed tooth in rats. PDLSC-CM downregulates the expression of HAPLN1 mainly in macrophages, thereby inhibits inflammation and osteoclastogenesis of delayed replanted tooth root. Overexpression of HAPLN1 abolishes the protective effect of PDLSC-CM on delayed replanted tooth root. CONCLUSION: HAPLN1 reduction in macrophages plays a pivotal role in PDLSC-CM reducing root resorption. PDLSC-CM is a promising preservation medium for avulsed teeth with potential clinical applications, and the development of drug candidate targeting HAPLN1 has favorable clinical prospects.
Adcyap1r1-driven astrocyte reprogramming attenuates neuroinflammation and promotes dopaminergic neuroprotection in Parkinson's Disease.
Zheng YY, Hu LR, Gu Y … +3 more , Cai MY, Wang XW, Chen WF
Stem Cell Res Ther · 2026 Jul · PMID 42393759 · Full text
BACKGROUND: Parkinson's disease (PD), the second most prevalent neurodegenerative disorder globally, is characterized by progressive degeneration of dopaminergic (DA) neurons and sustained neuroinflammatory cascades. Str...
BACKGROUND: Parkinson's disease (PD), the second most prevalent neurodegenerative disorder globally, is characterized by progressive degeneration of dopaminergic (DA) neurons and sustained neuroinflammatory cascades. Strategies that simultaneously suppress neuroinflammation and protect DA neurons are urgently needed, particularly through targeting astrocytes (As). Building on our previous discovery that combined miR-124 and small molecule interventions synergistically suppress As activation and induce their transdifferentiation into dopaminergic-like neurons, this study identified Adcyap1r1 as a pivotal regulator via RNA-seq analysis. Here, we systematically investigated its cAMP-mediated dual functional roles in neuroinflammatory modulation and DA neuron preservation. METHODS: TGF-β1-activated neonatal SD rat cortical reactive astrocytes (RAs) were used for Adcyap1r1 overexpression. We assessed astrocyte reactivity, neuroinflammation, neuron-like transition, and cAMP pathway activity in vitro. In MPTP-induced PD mice, AAV-mediated Adcyap1r1 overexpression was targeted to striatal As. Motor function, astrocyte activation, neuroinflammation, and endogenous DA neuron survival in the nigrostriatal system were evaluated through behavioral, histopathological, and molecular analyses. RESULTS: In activated RAs, Adcyap1r1 overexpression significantly attenuated reactivity, reduced pro-inflammatory mediator expression (e.g., COX-2, iNOS), activated cAMP signaling, and promoted the acquisition of a tyrosine hydroxylase-positive (TH) neuron-like phenotype. In MPTP-induced PD mice, astrocyte-targeted Adcyap1r1 overexpression in the striatum effectively inhibited astrocytic activation and neuroinflammation, protected endogenous TH neurons in the nigrostriatal system, and alleviated motor deficits, thereby supporting its DA neuroprotective potential. CONCLUSIONS: Our study demonstrates that Adcyap1r1 functions through a cAMP-dependent dual mechanism to suppress astrocyte reactivity and neuroinflammatory cascades, and facilitate the transition of RAs into a DA neuron-like phenotype. This dual regulatory mechanism protects the nigrostriatal DA system and ameliorates motor dysfunction in PD mice, providing a theoretical foundation for developing innovative therapeutic strategies against PD.
Differentiation of human induced pluripotent stem cells into cardiac valve cells using 2D and 3D differentiation protocols.
Farzaneh Z, Brückner A, Fleischmann BK … +1 more , Rieck S
Stem Cell Res Ther · 2026 Jul · PMID 42393756 · Full text
BACKGROUND: Given the high relevance of human cardiac valve disease, recent research aims to differentiate human induced pluripotent stem cells (hiPSCs) into valve endothelial-like cells (VELCs) and, through endothelial-...
BACKGROUND: Given the high relevance of human cardiac valve disease, recent research aims to differentiate human induced pluripotent stem cells (hiPSCs) into valve endothelial-like cells (VELCs) and, through endothelial-to-mesenchymal transition (EndMT), into valve interstitial-like cells (VILCs). METHODS: Here, we modified a 2D differentiation protocol demonstrating that VEGF can serve as the sole driver for differentiating cardiac progenitor cells (CPCs) into VELCs. Next, we utilized the so-called GiWi protocol (inhibition of glycogen synthase kinase, followed by inhibition of the Wnt pathway) to derive VELCs from 3D endocardial spheres. To this aim, hiPSCs were first differentiated into cardiac progenitor (CP) spheres using CHIR99021 (12 µM) and IWP2 (5 µM). Subsequent treatment with E8 medium containing high-dose FGF2 (100 ng/ml) resulted in endocardial spheres enriched for VELCs. For EndMT induction, endocardial spheres were MACS-sorted for PECAM1 VELCs and transdifferentiated into ACTA2/CDH5 VILCs using TGFβ1 (200 ng/ml). RESULTS: Using VEGF as main driver to differentiate CPCs into VELCs in 2D, the generated VELCs appeared stable over time, can be maintained in vitro and transdifferentiated into ACTA2 VILCs using FGF2 (100 ng/ml) and TGFβ1 (50 ng/ml). Besides, our novel 3D differentiation protocol yielded endocardial spheres, which were highly enriched with VELCs, as shown by the expression of GATA4 (≈ 83%), PECAM1 (≈ 69%), and nuclear NFATC1 (≈ 76%), along with typical functional characteristics such as network formation, LDL uptake and the ability to undergo EndMT. CONCLUSIONS: Overall, we developed a 2D differentiation protocol that produces stable VELCs and a high percentage of VILCs upon EndMT induction. We also established a new, efficient, and cost-effective protocol for the 3D differentiation of endocardial spheres to better mimic a physiologically relevant environment, thereby enabling improved maturation.
From monolayer to organoids and multi-organ microphysiological systems: advancing regenerative medicine and precision therapies.
Choudhery MS, Niaz A, Arif T … +1 more , Mahmood R
Stem Cell Res Ther · 2026 Jul · PMID 42387660 · Full text
BACKGROUND: The landscape of in vitro models has evolved from simple two dimensional (2D) cultures to three-dimensional (3D) organoids and multi-organ microphysiological systems. Early monolayer cultures enabled directed...
BACKGROUND: The landscape of in vitro models has evolved from simple two dimensional (2D) cultures to three-dimensional (3D) organoids and multi-organ microphysiological systems. Early monolayer cultures enabled directed differentiation but provided limited physiological relevance. MAIN BODY: The development of organoid technology is a significant invention, which allows the cells to self-organize into complex 3D structures to recapitulate the cell diversity, architecture and functions of natural tissues. This has enabled more effective modelling of patient-specific diseases and processes. The latest development of the multi-organ microphysiological systems, integrates organoids or engineered tissues with microfluidic channels through which nutrients are perfused, and blood flow as well as mechanical stimuli are mimicked. This technology provides precise control over the tissue microenvironment to facilitate dynamic cell interactions and communication among different tissue types. CONCLUSION: These platforms more precisely mimic human biological processes, thereby improving disease modelling, drug screening, and the development of tissue grafts for regenerative therapies. This review discusses the evolution from 2D monolayer cell cultures, through the formation of organoids, to the engineering of organ-on-a-chip systems. It underlines how these technologies have advanced regenerative therapies by enhancing the ability to repair or replace damaged tissues and precision medicine through the creation of patient-specific disease models and personalized treatment strategies. Importantly, this review provides a comparative critical assessment of the functional capabilities, limitations, and translational readiness of each platform, identifying the specific contexts in which each system excels or falls short of its alternatives.
Emerging roles of the long non-coding RNAs MALAT1 and TUG1 during differentiation of adipose tissue-derived mesenchymal stem cells towards insulin-producing cells.
Sanad EF, Saad AA, Rafeek J … +7 more , Mokbel R, Abdallah M, Emad N, Mohamed HA, Alaa Y, Mahmoud YM, Kassem DH
Stem Cell Res Ther · 2026 Jul · PMID 42387613 · Full text
BACKGROUND: Generation of insulin-producing cells (IPCs) from stem cells provides great hope for patients with diabetes mellitus (DM). Long non-coding RNAs (lncRNAs) ignited much interest regarding their role in determin...
BACKGROUND: Generation of insulin-producing cells (IPCs) from stem cells provides great hope for patients with diabetes mellitus (DM). Long non-coding RNAs (lncRNAs) ignited much interest regarding their role in determining the fate of stem cells. The lncRNAs MALAT1 and TUG1 have been reported to be interrelated with β-cell dysfunction and/or DM. However, their role during generation of IPCs from stem cells has not been adequately studied. Thus, the current study aimed to investigate the role of MALAT1 and TUG1 during differentiation of adipose tissue-derived mesenchymal stem cells (Ad-MSCs) towards IPCs. METHODS: Ad-MSCs were isolated from rat epididymal fat pads, characterized and induced to differentiate towards IPCs. Assessment of differentiation was done by measuring expression levels of various β-cell-related markers using RT-qPCR, as well as morphological changes, and dithizone staining. Expression levels of MALAT1 and TUG1 were also measured by RT-qPCR. Several in-silico analyses were done using RNA-protein Association and Interaction Networks (RAIN) database. RESULTS: MALAT1 and TUG1 expression levels were significantly increased during differentiation of Ad-MSCs into IPCs as compared to control uninduced cells. Furthermore, generated networks from RAIN database revealed an interplay between MALAT1 and TUG1, and between each of them with several common targets like GAS5, HOTAIR and TP53COR1. CONCLUSIONS: The current study portrays MALAT1 and TUG1 as novel interrelated molecular mediators and important regulatory nodes enhancing differentiation of Ad-MSCs towards IPCs. Their upregulation during differentiation can be interrelated with competitive endogenous RNA (ceRNA) networks, mediating various epigenetic modifications, orchestrating signaling pathways and overcoming cellular stress during reprogramming/differentiation.
SATB1 regulates the osteogenic differentiation of PDLSCs via HDAC1 mediated non-histone protein deacetylation and ubiquitination mechanism and through p38 MAPK pathway under hydrogen peroxide-induced senescent conditions.
Hu M, Song J, Yan W … +4 more , Jiang Y, Zhang C, Yang H, Fan Z
Stem Cell Res Ther · 2026 Jul · PMID 42387594 · Full text
BACKGROUND: Periodontitis is a chronic inflammatory disease that affects the supporting tissues around teeth. A reduction in the pluripotency of periodontal ligament stem cells (PDLSCs) has been identified as a pivotal f...
BACKGROUND: Periodontitis is a chronic inflammatory disease that affects the supporting tissues around teeth. A reduction in the pluripotency of periodontal ligament stem cells (PDLSCs) has been identified as a pivotal factor in age-related alveolar bone loss. This study investigated the effects of special AT-rich binding protein 1 (SATB1) on the osteogenic differentiation capacity of PDLSCs under HO-induced senescent conditions and its potential mechanisms, thereby providing new insights into periodontal regeneration in patients with periodontitis. METHODS: The osteogenic differentiation capacity of PDLSCs was determined by alkaline phosphatase (ALP) activity, alizarin red S (ARS) staining, and western blotting. Co-immunoprecipitation (Co-IP) was used to detect the binding of SATB1 to histone deacetylase 1 (HDAC1) and a ubiquitination assay was employed to detect the protein stability of SATB1. RESULTS: Under normal and HO-stimulation conditions, SATB1 enhances osteogenic differentiation of PDLSCs by activating the p38 mitogen-activated protein kinase (MAPK) and extracellular signal-regulated kinase (ERK) signaling pathways. The Co-IP results indicated that SATB1 could physically bind to HDAC1 and the binding of SATB1 and HDAC1 proteins decreased under HO-induced senescent conditions. In addition, HDAC1 promoted the expression of SATB1 and rescued the osteogenic differentiation capacity of PDLSCs via the activation of the p38 MAPK pathway under senescent conditions. Nevertheless, HDAC1 deacetylation mutant (HDAC1-H141A-MUT) did not affect the binding of SATB1 and HDAC1 but lost the effect of upregulating the expression of SATB1. Moreover, HDAC1-H141A-MUT lost the ability to promote the osteogenic differentiation of PDLSCs and the activation of the p38 MAPK signaling pathway. Furthermore, protein half-life experiments indicated that HDAC1 hindered the degradation of the SATB1 protein, whereas HDAC1-H141A-MUT lost this function. In the end, ubiquitination assay demonstrated that HDAC1 inhibited the ubiquitination of SATB1, while HDAC1-H141A-MUT has no effect on the ubiquitination of SATB1 protein. CONCLUSIONS: SATB1 modulated the osteogenic differentiation of PDLSCs through HDAC1 mediated non-histone protein deacetylation and ubiquitination and through the p38 MAPK pathway under HO-induced senescence conditions. Therefore, this new mechanism provides a feasible strategy for promoting periodontal tissue regeneration.
FGFR1 frameshift mutation mediates the dysfunction of mesenchymal stem cells in craniofacial microsomia.
Zhao S, Luo P, Ke C … +10 more , Li L, Li Z, Liu B, Ma L, Zang T, Li H, Xu X, He T, Wang B, Tang X
Stem Cell Res Ther · 2026 Jun · PMID 42380946 · Full text
Craniofacial microsomia represents a congenital craniofacial anomaly characterized by a complex etiology, the precise genetic determinants of CFM have remained largely elusive. Comprehensive exome sequencing analysis per...
Craniofacial microsomia represents a congenital craniofacial anomaly characterized by a complex etiology, the precise genetic determinants of CFM have remained largely elusive. Comprehensive exome sequencing analysis performed on a cohort of CFM patients has identified a specific pathogenic frameshift mutation (c.225dupA, p. I76fs) located within the Fibroblast Growth Factor Receptor 1 gene. Extensive functional characterization utilizing human umbilical cord-derived mesenchymal stem cells demonstrated that either the presence of this FGFR1 mutation or the targeted knockdown of FGFR1 significantly attenuated the endogenous expression of the receptor. This genetic perturbation was associated with a marked impairment of osteogenic differentiation potential, a substantial reduction in cellular proliferative and migratory capacities, and an exacerbated apoptotic response. From a mechanistic perspective, the disruption of FGFR1 function exerted a suppressive effect on pivotal signaling cascades essential for skeletal development, including the P38/ERK, Wnt/β-catenin, BMP2/SMAD4, and PI3K/AKT transduction axes. Furthermore, the integrity of critical molecular interactions between FGFR1 and structural co-factors, specifically vimentin, COL1A1, and FGF1, was compromised, resulting in a concomitant downregulation of their protein abundance. Collectively, these findings elucidate that the FGFR1 frameshift mutation is a significant contributor to the pathogenesis of CFM, principally by obstructing MSC-mediated osteogenesis through the dual disruption of essential signal transduction pathways and vital protein-protein interaction networks.
Intratympanic injection of human umbilical cord mesenchymal stem cell derived small extracellular vesicles for refractory sudden sensorineural hearing loss: a Phase 1 trial.
Shu F, Wu Y, Zhang Y … +7 more , Xu M, Zou T, Jiang S, Cai J, Bao J, Chen A, Zhang H
Stem Cell Res Ther · 2026 Jun · PMID 42380944 · Full text
BACKGROUND: Refractory sudden sensorineural hearing loss (RSSNHL) remains a therapeutic challenge with limited effective treatment options. Human umbilical cord mesenchymal stem cell-derived small extracellular vesicles...
BACKGROUND: Refractory sudden sensorineural hearing loss (RSSNHL) remains a therapeutic challenge with limited effective treatment options. Human umbilical cord mesenchymal stem cell-derived small extracellular vesicles (hucMSC-sEVs) have demonstrated otoprotective and regenerative potential in preclinical studies. This Phase 1 trial evaluated the safety of intratympanic hucMSC-sEVs in patients with RSSNHL. METHODS: This single-center, open-label, single-arm clinical study enrolled RSSNHL patients between June and September 2025 (ChiCTR2500103765). Participants received intratympanic hucMSC-sEVs for five consecutive days across four dose cohorts, ranging from 8 × 10⁸ to 1 × 10¹¹ particles/mL. Follow-up assessments were conducted at 1, 2, 4, and 8 weeks after treatment, during which adverse events (AEs) were recorded, and hearing outcomes were evaluated. RESULTS: Twelve of the thirteen enrolled patients completed the 8-week follow-up. Intratympanic administration of hucMSC-sEVs was well tolerated across all dose levels, with no dose-limited toxicity or serious AEs. The most common AEs were ear pain (5/12), ear fullness (3/12), and transient dizziness (2/12), all characteristic of intratympanic injection and resolving without intervention. CONCLUSIONS: In this Phase 1 study, intratympanic hucMSC-sEVs were well tolerated and showed preliminary signals of hearing improvement. Responses were observed only in patients receiving lower dose levels (8 × 10⁸ and 4 × 10⁹ particles/mL) and in those treated within a shorter disease window (≤ 22 days). These exploratory findings require confirmation in larger controlled trials. Trial Registration This study was registered on June 5,2025, at Chinese Clinical Trial Registry (ChiCTR2500103765).
Adipose stem cells derived extracellular vesicles alleviate retinal excitotoxicity via miR-23a-5p/PLCD1/PKCA/GluA2 axis: a potential therapeutic strategy.
Tianqi D, Huizhuo X, Shibo T … +4 more , Haiyang Y, Aixiang L, Ming L, Jufang H
Stem Cell Res Ther · 2026 Jun · PMID 42380927 · Full text
BACKGROUND: Despite excitotoxicity being a pivotal pathological mechanism in various retinal diseases, effective clinical interventions remain limited. Previous study has shown that adipose stem cell-derived extracellula...
BACKGROUND: Despite excitotoxicity being a pivotal pathological mechanism in various retinal diseases, effective clinical interventions remain limited. Previous study has shown that adipose stem cell-derived extracellular vesicles (ADSC-EVs) can alleviate glutamate-induced retinal ganglion cells (RGCs) death by suppressing protein kinase C alpha (PKCA) pathway and increasing the expression of α-amino-3-hydroxy-5-methyl-4-isoxazoleproprionic acid receptors (AMPARs) subunit 2 (GluA2) on the cell membrane, but the mechanisms remain unexplored. METHODS: To clarify the molecular processes involved in ADSC-EVs-mediated intracellular calcium balance, we isolated ADSC-EVs using ultrafiltration and ultracentrifugation, and characterized these vesicles by transmission electron microscopy, nanoparticle tracking analysis, and flow cytometry. Small RNA sequencing was performed on glutamate-injured rat retinal precursor (R28) cells pre-treated with ADSC-EVs or PBS. Through bioinformatic analysis, we identified candidate microRNAs and predicted their potential target genes. The regulatory effects of microRNA were confirmed using propidium iodide staining, Fluo-4AM staining, western blotting, and immunofluorescence. Additionally, the RGCs counting and visual function tests were employed to evaluate the therapeutic efficacy of the microRNA in the glutamate-induced SD rat - animal model. RESULTS: Our results demonstrated that pre-treatment with ADSC-EVs led to a significant increase in the expression levels of miR-127-3p, miR-181b-1-3p, miR-199a-3p/5p, miR-23a-5p, miR-23b-5p, and miR-486 in R28 cells. Bioinformatic analyses suggest that miR-23a-5p may contribute to regulating the calcium overload by inhibiting the expression of phospholipase C delta 1 (PLCD1). Overexpression of miR-23a-5p or pre-treatment with ADSC-EVs modulated the expression of GluA2 on the cell membrane through inhibiting the PLCD1/PKCA/GluA2 axis, thereby reducing intracellular calcium levels and diminishing R28 cell death. In contrast, inhibition of miR-23a-5p expression partially reversed the regulatory effects of ADSC-EVs on calcium concentration and cell viability. Furthermore, our findings suggest that overexpression of miR-23a-5p in retina alleviated glutamate-induced RGCs death and visual function impairment, whereas suppression of miR-23a-5p exacerbated glutamate-induced RGCs death. CONCLUSION: ADSC-EVs delived miR-23a-5p mitigate glutamate-induced RGCs damage by inhibiting the PLCD1/PKCA/GluA2 axis. Targeting this miR-23a-5p-mediated axis may therefore represent a promising therapeutic approach for excitotoxic RGCs injury.
Orthodontic loading modulates epithelial progenitor dynamics and enamel formation in the mouse mandibular incisor.
Bar On I, Klein Y, Shahin E … +5 more , Asmar J, Takano S, Hu JK, Chaushu S, Sharir A
Stem Cell Res Ther · 2026 Jun · PMID 42380895 · Full text
BACKGROUND: Adult stem cells (SCs) maintain tissue homeostasis through a balance of self-renewal and differentiation regulated by biochemical and mechanical cues. While biochemical pathways are well studied, the in vivo...
BACKGROUND: Adult stem cells (SCs) maintain tissue homeostasis through a balance of self-renewal and differentiation regulated by biochemical and mechanical cues. While biochemical pathways are well studied, the in vivo mechanisms by which external forces influence SCs and their progeny remain poorly understood. The continuously growing mouse incisor offers a tractable model for investigating these mechanisms because dental epithelial stem cells (DESCs) reside in a spatially restricted apical niche, and their progeny undergo stereotyped proliferation and differentiation along the apical-incisal axis. We investigated how intrusive mechanical loading affects dental epithelial cell kinetics and enamel regeneration during injury repair. METHODS: A modified orthodontic tooth movement device was adapted to apply controlled intrusive forces (0.05-0.5 N) to the mouse mandibular incisor. To stimulate regeneration, the incisal tip was trimmed, and mice were subjected to force application for three days, followed by recovery after device removal. Dental epithelial responses were evaluated using histology, dual EdU/BrdU labeling, in situ hybridization, and micro-computed tomography. Expression of proliferation (Ccnb1) and differentiation (Igfbpl1) markers, as well as nuclear localization of the mechano-responsive transcription co-factor YAP, were analyzed. RESULTS: Forces ≥ 0.2 N caused adverse health effects, whereas 0.05 N induced consistent epithelial changes without systemic consequences. At 0.05 N loading, incisors showed delayed regeneration and hypomineralized enamel. The apical epithelium exhibited folds, tears, reduced proliferation, and premature amelogenin expression. These effects reversed after load removal, coinciding with restored proliferation and enamel deposition. Gene expression analysis revealed apical-incisal shifts in Ccnb1 and Igfbpl1 domains, consistent with altered cell kinetics. Mechanistically, loading decreased nuclear YAP localization in the central body of the labial cervical loop, suggesting a role for this mechanosensitive pathway in mediating the cellular response to mechanical force. CONCLUSIONS: This study presents an in vivo model for examining mechanical influences on dental epithelial progenitor cells. Intrusive loading suppresses proliferation, promotes precocious differentiation, and alters epithelial architecture. These findings support a role for mechanical cues in modulating tissue regeneration and provide a framework for future mechanistic studies in tooth biology.
Correction: Essential role of p21 in the modulation of post-traumatic hippocampal Neural Stem Cells response.
Chiani F, Mastrorilli V, Marchetti N … +11 more , Macioce A, Nappi C, Strimpakos G, Pasquini M, Gambadoro A, Battistini JI, Cutuli D, Petrosini L, Marinelli S, Scardigli R, Vecchioli SF
Stem Cell Res Ther · 2026 Jun · PMID 42374492 · Full text
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