International Journal Of Molecular Medicine[JOURNAL]
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200 papers
Dysregulation of the DNA repair‑immune axis: Targeted therapeutic strategies for autoimmune diseases (Review).
Wan K, Wang M, Xia Q … +9 more , Fang H, Chen Y, Zhou T, Yang X, Wang L, Ye J, Shu H, Li XF, Li J
Int J Mol Med · 2026 Jun · PMID 42028743 · Full text
DNA damage and repair mechanisms are crucial for maintaining genomic stability, and their dysregulation is closely linked to the complex pathogenesis of autoimmune diseases. The present review systematically describes th...
DNA damage and repair mechanisms are crucial for maintaining genomic stability, and their dysregulation is closely linked to the complex pathogenesis of autoimmune diseases. The present review systematically describes the types of DNA damage, key repair pathways, their regulatory networks, and the multidimensional interactions between DNA repair and the immune system. Furthermore, it delves into how defective DNA repair drives the development of autoimmune disorders such as systemic lupus erythematosus and rheumatoid arthritis through mechanisms encompassing cyclic GMP‑AMP synthase (cGAS)‑stimulator of interferon genes (STING) pathway activation, self‑antigen release and breakdown of immune tolerance. Oxidative stress‑induced DNA damage, mutations in repair genes and aberrant accumulation of cytosolic DNA are key triggers of autoimmune responses. In addition, DNA repair proteins indirectly influence disease progression by modulating immune cell functions, including T‑cell homeostasis and macrophage polarization. The present review further summarizes the therapeutic potential and challenges of targeting DNA damage response pathways, including via poly adenosine diphosphate ribose polymerase inhibitors and cGAS‑STING axis regulation, as demonstrated in pre‑clinical models. Future research leveraging multi‑omics and innovative delivery systems will be crucial for translating these discoveries into effective, personalized therapies. The present review advances the development of personalized precision medicine and provides a solid theoretical foundation for developing novel treatment strategies.
RNA‑binding proteins as epithelial transcriptome orchestrators in gastric cancer: Immune‑metabolic crosstalk and therapeutic vulnerability (Review).
Liu S, Ma Z, Ji B … +6 more , Zhu J, Yao S, Terai S, Tuo B, Li T, Liu X
Int J Mol Med · 2026 Jun · PMID 41992985 · Full text
Among malignant tumors, gastric cancer (GC) ranks fifth in terms of global incidence and third in terms of the number of related deaths, and its high molecular heterogeneity, chemoresistance and lack of targeted therapie...
Among malignant tumors, gastric cancer (GC) ranks fifth in terms of global incidence and third in terms of the number of related deaths, and its high molecular heterogeneity, chemoresistance and lack of targeted therapies remain major clinical challenges. RNA‑binding proteins (RBPs), as the core effectors in post‑transcriptional regulation, are widely involved in the determination of malignant phenotypes in GC; they act by dynamically regulating RNA splicing, stability, translation and modification, in addition to mediating the crosstalk between metabolism and immunity, and influencing proliferation, metastasis, drug resistance and other malignant phenotypes. However, the functional controversy of RBPs [such as Insulin‑like growth factor 2 mRNA‑binding protein 1 (IGF2BP1) and YTH N6‑methyladenosine RNA binding protein F2 (YTHDF2)] in different GC subtypes and their clinical translatability remain unclear. Notably, RBPs show GC‑specific features (such as IGF2BP1/3 regulating metabolic coupling, YTHDF1 modulating dendritic cell recruitment) and clinical value [such as poly (rC)‑binding protein predicting peritoneal metastasis, Pumilio 1 guiding anti‑programmed cell death protein 1 therapy therapy]. This review highlights the GC‑specific mechanisms, controversial scientific issues and latest clinical translation progress of RBPs and proposes personalized treatment strategies based on the molecular characteristics of RBPs, aiming to provide a theoretical and practical basis for overcoming GC chemoresistance and molecular heterogeneity.
ETS‑1/ETS‑2 transcription factors in CVD (Review).
Yang S, Zhang J, Yang Y … +3 more , Lv Y, Yang J, Wang H
Int J Mol Med · 2026 Jun · PMID 41992981 · Full text
Cardiovascular diseases remain the leading cause of global morbidity and mortality, imposing a significant burden on families and societies. E26 transformation‑specific (ETS)‑1 and ETS‑2, members of the ETS family of tra...
Cardiovascular diseases remain the leading cause of global morbidity and mortality, imposing a significant burden on families and societies. E26 transformation‑specific (ETS)‑1 and ETS‑2, members of the ETS family of transcription factors (also known as proto‑oncogenes), are increasingly recognized for their roles in tumor progression. Recent studies highlight their importance in normal coronary artery development, myocardial homeostasis and the regulation of vascular inflammation and remodeling. Emerging evidence suggests that ETS‑1/ETS‑2 are critical in the pathogenesis of atherosclerosis, myocardial ischemia‑reperfusion injury, cardiac remodeling and heart failure. The present review summarized the research progress of ETS‑1/ETS‑2 in cardiovascular diseases, discusses the relevant challenges encountered in the translational process of ETS‑1/ETS‑2‑targeted therapy for cardiovascular diseases and provides novel strategies for the treatment of cardiovascular diseases targeting ETS‑1/ETS‑2.
IDH2 lactylation regulates mitochondrial dysfunction injury induced by myocardial ischemia‑reperfusion via the AMPK signaling pathway.
Wang C, Shen S, Chen S … +9 more , Lin J, Li S, Chen J, Cai S, Yuan X, Yang Z, Ding K, Xu L, Zhang L
Int J Mol Med · 2026 Jun · PMID 41992974 · Full text
Ischemic cardiomyopathy ranks as a principal cause of death and incapacity worldwide. Myocardial ischemia‑reperfusion injury (MIRI) caused by percutaneous coronary intervention is a major threat in the treatment of ische...
Ischemic cardiomyopathy ranks as a principal cause of death and incapacity worldwide. Myocardial ischemia‑reperfusion injury (MIRI) caused by percutaneous coronary intervention is a major threat in the treatment of ischemic cardiomyopathy. Although lactylation (Kla) is extensively implicated in numerous pathological processes, its role and specific effects in MIRI remain unclear. Lactylation proteomics was used to identify proteins with different modifications during ischemia‑reperfusion injury. Co‑immunoprecipitation experiments were utilized to detect isocitrate dehydrogenase 2 (IDH2) lactylation levels. Immuno-fluorescence staining was applied to confirm intracellular lactylation levels. TUNEL, DHE and MitoSOX staining were used to measure oxidative damage in cells and tissues. An oxygen consumption rate experiment and the ATP assay were conducted to determine mitochondrial function. Western blots were utilized to detect changes in proteins related to mitochondrial functional homeostasis and downstream signal alterations. Excessive lactate accumulation was observed in MIRI model mice. This accumulation exacerbated the decline in cardiac function and the damage to cardiomyocytes in mice after MIRI. The lactylation of IDH2 in mitochondria was found to play a regulatory role in mitochondrial dysfunction and MIRI. Regarding the mechanism, it was verified that high IDH2 K275 lactylation caused a reduction in its enzymatic activity and decreased the production of α‑ketoglutarate in the tricarboxylic acid cycle. Consequently, the activation of the AMPK pathway was inhibited, and mitochondrial damage and functional impairment were aggravated. It was also found that SIRT3 regulated and prevented IDH2 lactylation. The results of the present study indicated that IDH2 lactylation, which is elevated due to lactate accumulation and negatively regulated by SIRT3, contributes to the exacerbation of MIRI by regulating the functional homeostasis of mitochondria. This discovery offers a new therapeutic concept and target for MIRI prevention.
Triptolide exerts antiviral effects and alleviates influenza A‑induced pneumonia by inhibiting the overactivation of absent in melanoma 2 signaling in immune cells.
Chen Y, Wu H, Wu X … +7 more , Che L, Fu X, Qi R, Jia D, Li M, Xie W, Zhu W
Int J Mol Med · 2026 Jun · PMID 41992969 · Full text
Influenza A (H1N1) virus‑induced pneumonia poses a significant clinical challenge because of excessive immune activation and limited targeted therapies. While current antivirals suppress viral replication, they fail to c...
Influenza A (H1N1) virus‑induced pneumonia poses a significant clinical challenge because of excessive immune activation and limited targeted therapies. While current antivirals suppress viral replication, they fail to control absent in melanoma 2 (AIM2) inflammasome‑mediated hyperinflammation, a key driver of immunopathology and mortality. The present study investigated whether triptolide (TP) ameliorates H1N1‑induced pneumonia by targeting this unmet need. The results demonstrated that H1N1 infection reduced the levels of inflammatory cytokines in both human bronchial epithelial cells (HBEpiCs) and THP‑1 cells and decreased the adhesion between the two cell types. Furthermore, high‑dose H1N1 activation triggered the AIM2 signaling pathway in THP‑1 cells but not in HBEpiCs and decreased the viability of THP‑1 cells. and experiments both confirmed that TP effectively inhibited inflammation in alveolar epithelial cells and immune cells, as well as the adhesion between these cell types. Additionally, TP reduced the viral load of H1N1 in a murine pneumonia model. Further studies revealed that TP inactivated the AIM2 signaling pathway in THP‑1 cells but not in HBEpiCs. However, overexpression of AIM2 in THP‑1 cells markedly reversed the anti‑inflammatory effects of TP. Based on these findings, it was hypothesized that TP modulates the immune response by inactivating the AIM2 signaling pathway in immune cells, which reduces excessive immune cell activation and decreases the harmful interactions between immune cells and alveolar epithelial cells, ultimately alleviating the lung inflammation induced by H1N1 virus infection. The present study proposed a novel mechanism by which TP alleviates lung damage by suppressing AIM2‑driven immune hyperactivation in immune cells, thereby reducing harmful crosstalk with epithelial cells. This is the first evidence of AIM2‑targeted therapy positioning TP as a promising candidate for treating viral pneumonia.
Glycolytic lactylation modulates cell death decisions in diabetic kidney disease: Metabolic‑epigenetic interplay between ferroptosis and autophagy in fibrotic remodeling (Review).
Zhang T, Zhang X, Xie Y … +5 more , Liu Y, Xia S, Yin X, Li T, Liao L
Int J Mol Med · 2026 Jun · PMID 41992968 · Full text
Diabetic kidney disease (DKD), a predominant contributor to end‑stage renal disease, is distinguished by its intricate pathogenesis and constrained therapeutic interventions. The present review discusses the role of glyc...
Diabetic kidney disease (DKD), a predominant contributor to end‑stage renal disease, is distinguished by its intricate pathogenesis and constrained therapeutic interventions. The present review discusses the role of glycolytic flux‑mediated protein lactylation, an emerging epigenetic modification, in the progression of DKD. Under conditions of hyperglycemia and hypoxia, renal cells undergo a metabolic shift towards glycolysis, resulting in the accumulation of lactate. Beyond its role as a metabolic byproduct, lactate functions as a signaling molecule that facilitates the lactylation of both histones and non‑histone proteins. The present review discusses how lactylation has been implicated in key pathological mechanisms in DKD, including ferroptosis, dysregulated autophagy and fibrosis. The interplay between lactylation and other posttranslational modifications is also discussed, along with the therapeutic potential of targeting the glycolysis‑lactylation axis. By highlighting this metabolic‑epigenetic crosstalk, the present review proposes a conceptual framework that may inform the development of diagnostic and therapeutic strategies targeting lactylation in DKD.
[Retracted] Quercetin promotes the apoptosis of fibroblast‑like synoviocytes in rheumatoid arthritis by upregulating lncRNA MALAT1.
Pan F, Zhu L, Lv H … +1 more , Pei C
Int J Mol Med · 2026 Jun · PMID 41992966 · Full text
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data featured in Figs. 2 and 5, and the control western blot data in Fig. 6A were...
Following the publication of this paper, it was drawn to the Editor's attention by a concerned reader that certain of the flow cytometric data featured in Figs. 2 and 5, and the control western blot data in Fig. 6A were strikingly similar to data which had been already been submitted for publication in articles that were written by different authors at different research institutes. Owing to the fact that the contentious flow cytometric and western blot data in the above article were found to be strikingly similar to data that had already been submitted for publication elsewhere, the Editor of has decided that this paper should be retracted from the Journal. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a reply. The Editor apologizes to the readership for any inconvenience caused. [International Journal of Molecular Medicine 38: 1507‑1514, 2016; DOI: 10.3892/ijmm.2016.2755].
Context‑dependent duality of the apelin/elabela‑APJ system in diabetes and its complications (Review).
Han Z, Zhang J, Shi M … +4 more , Chen J, Li A, Ye Y, Zhang H
Int J Mol Med · 2026 Jun · PMID 41992965 · Full text
The apelin/elabela‑apelin receptor (APJ) signaling system is a key regulator of metabolic homeostasis and cardiovascular function in diabetes mellitus. However, its therapeutic application is complicated by its functiona...
The apelin/elabela‑apelin receptor (APJ) signaling system is a key regulator of metabolic homeostasis and cardiovascular function in diabetes mellitus. However, its therapeutic application is complicated by its functional divergence: the system exerts protective effects in some tissues while driving pathology in others. The present review examined these distinct roles, focusing on how the biological outcome depends on the specific ligand, disease stage and tissue microenvironment. It discussed the molecular mechanisms underlying this divergence, as well as the varying roles of the same receptor at different stages of the same disease. Finally, it evaluated emerging therapeutic strategies, such as stabilized analogs and biased agonists, proposing that precise targeting of the APJ conformational landscape offers a pathway to move beyond glycemic control toward multi‑organ protection in diabetes.
[Retracted] Role of miR‑146a in human chondrocyte apoptosis in response to mechanical pressure injury .
Jin L, Zhao J, Jing W … +4 more , Yan S, Wang X, Xiao C, Ma B
Int J Mol Med · 2026 Jun · PMID 41952503 · Full text
Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the Smad4, VEGF and GAPDH protein bands featured in Figs. 3D, 5C and F, 8D and 10B appeared to be striking...
Following the publication of the above article, a concerned reader drew to the Editor's attention that certain of the Smad4, VEGF and GAPDH protein bands featured in Figs. 3D, 5C and F, 8D and 10B appeared to be strikingly similar, suggesting that the data featured in the affected figure parts had been erroneously assembled. After having conducted an internal investigation of the data in this paper in the Editorial Office, the findings of the reader were found to be largely confirmed; in particular, it was noted that the western blots featured in Figs. 5C, 5F and 10B were strikingly similar, even though the orientation of the bands differed in some of the gel slices, such that data which were intended to show the results of differently performed experiments had apparently all been derived from the same original source. Given the large number of identifications of overlapping and/or re‑used western blot data in this paper, the Editor of has determined that this paper should be retracted from the Journal on the grounds of an overall lack of confidence in the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office did not receive a satisfactory reply. The Editor sincerely apologizes to the readership for any incovenience caused, and we thank the reader for drawing this matter to our attention. [International Journal of Molecular Medicine 34: 451‑463, 2014; DOI: 10.3892/ijmm.2014.1808].
A tale of dual role: HECT‑type E3 ubiquitin ligase mechanisms in liver diseases (Review).
Li T, Chen H, Zhao P … +2 more , Yin C, Song Z
Int J Mol Med · 2026 Jun · PMID 41952501 · Full text
HECT‑type E3 ubiquitin ligases play crucial and complex roles in liver diseases such as metabolic dysfunction‑associated steatotic liver disease (MASLD), metabolic dysfunction‑associated steatohepatitis (MASH), liver fib...
HECT‑type E3 ubiquitin ligases play crucial and complex roles in liver diseases such as metabolic dysfunction‑associated steatotic liver disease (MASLD), metabolic dysfunction‑associated steatohepatitis (MASH), liver fibrosis, viral hepatitis and hepatocellular carcinoma (HCC). In MASLD/MASH, these enzymes regulate lipid homeostasis and inflammatory signaling through bidirectional modulation of key metabolic pathways, including PPARα‑SREBP, JAK‑STAT and MAPK cascades. During liver fibrosis, specific HECT members simultaneously promote TGF‑β/Smad signaling by ubiquitinating Smad7 while limiting extracellular matrix deposition through the degradation of TGF‑β receptors. In viral hepatitis, they restrict viral replication via direct ubiquitination and proteasomal degradation of viral proteins yet concurrently facilitate viral release by hijacking the host ESCRT machinery. In HCC, these ligases critically influence tumor progression through opposing mechanisms: Acting as oncogenic drivers by destabilizing tumor suppressors such as PTEN, while functioning as tumor suppressors by degrading oncoproteins including c‑Myc and β‑catenin to attenuate proliferative signaling. Collectively, the 'dual‑role' behavior of HECT‑type E3 ligases is governed by disease‑specific contexts, substrate selection, ubiquitin linkage type (K48 vs. K63), and integration of microenvironmental cues. Although this functional duality presents significant translational challenges, understanding these dual regulatory networks provides critical insights into the pathogenesis of liver diseases and reveals potential avenues for targeted interventions.
Macrophage metabolism reprogramming in sepsis: Pathogenesis and therapeutic implications (Review).
Zhao T, Zhang W, Ren Z … +1 more , Feng X
Int J Mol Med · 2026 Jun · PMID 41930580 · Full text
Sepsis is a life‑threatening syndrome of organ dysfunction caused by infection, characterized by complex pathogenesis and high clinical mortality. As innate immune cells, macrophages serve a pivotal role in the initiatio...
Sepsis is a life‑threatening syndrome of organ dysfunction caused by infection, characterized by complex pathogenesis and high clinical mortality. As innate immune cells, macrophages serve a pivotal role in the initiation, progression and resolution of sepsis. The present review focuses on the key molecular nodes and signaling pathways of macrophage metabolic reprogramming in the process of sepsis. Key mechanisms include: i) The mammalian target of rapamycin‑hypoxia inducible factor‑1α (HIF‑1α)‑pyruvate kinase M2 axis as the primary regulator of glycolytic flux and pro‑inflammatory cytokine production; ii) tricarboxylic acid cycle interruption leading to succinate accumulation, which amplifies HIF‑1a signaling and promotes interleukin‑1β release via G protein‑coupled receptor 91, thereby exacerbating inflammation; iii) triggering receptor expressed on myeloid cells 2‑SH2‑containing protein tyrosine phosphatase‑1 axis‑mediated impairment of fatty acid oxidation, promoting lipid accumulation and pro‑inflammatory activation; and iv) amino acid depletion contributing to immune paralysis. In view of the 31.5% global mortality (21.4 million mortalities in 2021) caused by sepsis, a shift from supportive treatment to precise immune metabolism intervention is needed. The present article uniquely integrates the coordinated regulation of glucose, lipid and amino acid metabolic networks of macrophages in sepsis, and expounds the research status of immune metabolism in sepsis, in order to provide reference for the clinical treatment of sepsis. Targeted modulation of macrophage metabolism offers a new direction for individualized immunometabolic therapy in sepsis.
Animal models accurately representing acute liver failure (Review).
Luo S, Wu F, Jin Y … +3 more , Huang X, Liu D, Tian B
Int J Mol Med · 2026 Jun · PMID 41930578 · Full text
Animal models are essential for investigating disease pathogenesis and progression. Acute liver injury (ALI) precedes acute liver failure (ALF), establishing a crucial and close relationship between these conditions. App...
Animal models are essential for investigating disease pathogenesis and progression. Acute liver injury (ALI) precedes acute liver failure (ALF), establishing a crucial and close relationship between these conditions. Appropriate animal models are required in order to develop successful treatments for ALF. However, the inability to construct appropriate animal models that accurately represent the pathophysiological features of ALF has impeded research progress. The present review examined the pathophysiological mechanisms of ALF, evaluated the strengths and limitations of commonly used model organisms, and highlighted the advantages of mouse models in simulating the onset and progression of ALF. Furthermore, the review systematically summarized the varying drug and chemical dosages used in the development of drug‑induced and chemical‑induced ALF models in mice. In addition, whether ALI/ALF models constructed with different drug dosages accurately reflect disease progression has been a topic of critical discussion. Therefore, the present review proposed specific drug and chemical dosages for ALF model development and described future directions for developing optimal ALF animal models.
[Expression of Concern] DTX3L is upregulated in glioma and is associated with glioma progression.
Xu P, Tao X, Zhao C … +11 more , Huang Q, Chang H, Ban N, Bei Y, Xia X, Shen C, Wang K, Xu L, Wu P, Ren J, Wang D
Int J Mol Med · 2026 Jun · PMID 41930575 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the paraffin‑embedded glioma tissue sections shown in Fig. 2A on p. 494, the Ki‑67/Grade III and...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that, regarding the paraffin‑embedded glioma tissue sections shown in Fig. 2A on p. 494, the Ki‑67/Grade III and DTX3L/Grade IV data panels contained an overlapping section, suggesting that these data panels were derived from the same original source where different experimental groups were reported. In addition, GAPDH control western blots featured in Figs. 1C and 4E were found to be strikingly similar, even though the experimental conditions reported for these figure parts were different. The authors have been contacted by the Editorial Office to offer an explanation for these apparent anomalies in the presentation of the data in their paper, and we are awaiting their response. Due to the fact that we have been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of these potential problems while the Editorial Office continues to investigate this matter further. [International Journal of Molecular Medicine 40: 491‑498, 2017; DOI: 10.3892/ijmm.2017.3023].
[Corrigendum] Influence of aspirin on the CX3CL1/CX3CR1 signaling pathway in acute pulmonary embolism.
Zhang Z, Yang W, Ying R … +6 more , Shi Y, Jiang H, Cai D, Kuang J, Yang R, Wang L
Int J Mol Med · 2026 Jun · PMID 41930567 · Full text
Following the publication of the above article, an interested reader drew to the authors' attention that, concerning the images showing the construction of the CX3CL1‑over-expression adenovirus and the CX3CL1 short hairp...
Following the publication of the above article, an interested reader drew to the authors' attention that, concerning the images showing the construction of the CX3CL1‑over-expression adenovirus and the CX3CL1 short hairpin RNA (shRNA) adenovirus in Fig. 1 on p. 1581, the 'P3x100, Ad‑CX3CL1 OE' data panel in Fig. 1A contained an overlapping section with the 'P3x100, Ad‑CX3CL1 shRNA1' data panel in Fig. 1B, such that these were apparently derived from the same original source where different experiment conditions were reported. In addition, for the lung pathology images shown in Fig. 3 on p. 1584, the images showing the 'ASPx100' and the 'M+Ax100' experiments were apparently identical, suggesting that this figure had also been assembled incorrectly. After re‑examining their original data, the authors regret that Figs. 1 and 3 did contain errors in terms of their assembly, as identified by the external reader. Concerning Fig. 1, the authors wish to point out that these experiments were performed by the virus packaging company (Hanbio Biotechnology), who acknowledged that they were responsible for the error that was made in the provision of the images for this figure. Moreover, this error did not have any real significance in terms of the reported reports in this study, since neither shRNA1 nor shRNA2 was ultimately selected as the vector for the subsequent experiments; shRNA3 was selected as the interference vector of choice. Therefore, the Editor has approved the inclusion of a new version of Fig. 1 in this Corrigendum, comprising only the data for shRNA3 in Fig. 1B.Regarding Fig. 3, the revised version of this is also shown in the subsequent pages, showing the correct data for the 'Nx100', 'ASPx100' and 'M+Ax100' panels. Note that the revisions made to these figures do not affect the overall conclusions reported in the paper. The authors express their gratitude to the Editor of for allowing them the opportunity to publish this corrigendum, and apologize to the readership for any inconvenience caused. [International Journal of Molecular Medicine 39: 1580‑1588, 2017; DOI: 10.3892/ijmm.2017.2969].
[Corrigendum] Macrophage‑derived foam cells impair endothelial barrier function by inducing endothelial‑mesenchymal transition via CCL‑4.
Yang Y, Luo NS, Ying R … +13 more , Xie Y, Chen JY, Wang XQ, Gu ZJ, Mai JT, Liu WH, Wu MX, Chen ZT, Fang YB, Zhang HF, Zuo ZY, Wang JF, Chen YX
Int J Mol Med · 2026 Jun · PMID 41930563 · Full text
Following the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 3 on p. 563, the cell morphological images shown for Fig. 3E and F, representing the results for M2a‑ and...
Following the publication of the above article, an interested reader drew to the authors' attention that, in Fig. 3 on p. 563, the cell morphological images shown for Fig. 3E and F, representing the results for M2a‑ and M2c‑derived foam cells respectively, contained an overlapping section, such that data which were intended to show the results from differently performed experiments had apparently been derived from the same original source. 0The authors were able to consult their original data, and realized that the data panel shown to represent Fig. 3E had inadvertently been included in this figure erroneously. The revised version of Fig. 3, now showing the correct data for Fig. 3E, is shown on the next page. The authors can confirm that the error associated with this figure did not have any significant impact on either the results or the conclusions reported in this study, and all the authors agree with the publication of this Corrigendum. The authors are grateful to the Editor of for allowing them the opportunity to publish this Corrigendum; furthermore, they apologize to the readership of the Journal for any inconvenience caused. [International Journal of Molecular Medicine 40: 558‑568, 2017; DOI: 10.3892/ijmm.2017.3034].
Targeting pyroptosis to treat aortic aneurysms: From mechanism to drug discovery (Review).
Mao J, Luo M, Ruan L … +1 more , Zhang C
Int J Mol Med · 2026 Jun · PMID 41930562 · Full text
Pyroptosis is a lytic and highly inflammatory type of programmed cell death that is mediated primarily by members of the gasdermin (GSDM) protein family. Upon activation by inflammatory stimuli or danger signals, GSDMs a...
Pyroptosis is a lytic and highly inflammatory type of programmed cell death that is mediated primarily by members of the gasdermin (GSDM) protein family. Upon activation by inflammatory stimuli or danger signals, GSDMs are cleaved to release N‑terminal fragments that oligomerize and form pores in the plasma membrane. This disrupts cellular integrity, resulting in osmotic lysis and the release of potent proinflammatory cytokines, such as interleukin (IL)‑1β and IL‑18. The progression of an aortic aneurysm (AA) is driven by complex pathophysiological processes, with the loss of vascular smooth muscle cells and sustained vascular inflammation being central to disease pathogenesis. Emerging evidence indicates that pyroptosis markedly contributes to AA development by amplifying inflammatory activation and promoting cellular disintegration within the aortic wall. Further preclinical evidence has demonstrated that pharmacological inhibition of key pyroptosis signaling pathways effectively attenuates AA formation in murine models, underscoring its promising therapeutic potential. The present review summarizes the molecular mechanisms of pyroptosis, highlights its pathophysiological role in AAs and discusses novel therapeutic strategies targeting pyroptosis for the treatment of AAs.
Role of aging‑related cytokines in neurodegenerative disease (Review).
Dai X, Rao X, Wang Y … +1 more , Zhao W
Int J Mol Med · 2026 Jun · PMID 41930561 · Full text
Neurodegenerative diseases (NDs) are neurological disorders marked by neuronal damage and functional decline, notably affecting human quality of life and imposing substantial burdens on healthcare systems. The increasing...
Neurodegenerative diseases (NDs) are neurological disorders marked by neuronal damage and functional decline, notably affecting human quality of life and imposing substantial burdens on healthcare systems. The increasing prevalence of NDs is associated with intensification of population aging worldwide. Consequently, there is need to investigate effective prevention and treatment strategies. Aging is a risk factor for NDs. Throughout the aging process, alterations in the expression of specific cytokines occur, such as IL‑6 and tumor necrosis factor‑α, precipitating a cascade of chronic inflammatory responses. The present study provides a comprehensive review of the alterations in cytokines associated with aging in NDs and the chronic inflammatory responses they elicit. Furthermore, it explores the mechanisms by which these cytokines contribute to neuroinflammation, neuronal damage and cell death, thereby proposing a novel research direction for the treatment of NDs through cytokine regulation.
[Expression of Concern] Increased expression of heat shock protein 90 under chemical hypoxic conditions protects cardiomyocytes against injury induced by serum and glucose deprivation.
Wu K, Xu W, You Q … +4 more , Guo R, Feng J, Zhang C, Wu W
Int J Mol Med · 2026 Jun · PMID 41930560 · Full text
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the HSP90 blots shown in Figs. 2A and 4A on p. 1140 were strikingly similar after horizontally flipping, and...
Following the publication of the above paper, it was drawn to the Editor's attention by a concerned reader that the HSP90 blots shown in Figs. 2A and 4A on p. 1140 were strikingly similar after horizontally flipping, and then horizontally and vertically resizing, the bands in Fig. 2A, suggesting that these data panels were derived from the same original source where different experimental groups were reported. The authors have been contacted by the Editorial Office to offer an explanation for this apparent anomaly in the presentation of the data in their paper, and we are awaiting their response. Due to the fact that we have been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [International of Molecular Medicine 30: 1138‑1144, 2012; DOI: 10.3892/ijmm.2012.1099].
Astragaloside IV targets TUBB4B to inhibit proliferation and promote apoptosis of pituitary tumor cells via the STMN1/ERK pathway.
Li J, Qu Y, Zhang W … +5 more , Yang Z, Zeng Y, Xu J, Xie K, Liu Q
Int J Mol Med · 2026 Jun · PMID 41930558 · Full text
Pituitary tumors, as common intracranial neoplasms, present challenges in clinical management because of high postoperative recurrence rate, drug resistance and pronounced side effects. Astragaloside IV (AS‑IV), the prim...
Pituitary tumors, as common intracranial neoplasms, present challenges in clinical management because of high postoperative recurrence rate, drug resistance and pronounced side effects. Astragaloside IV (AS‑IV), the primary active component of the traditional Chinese herb , has antitumor activity in numerous types of cancer. However, its effects and mechanisms in pituitary tumors remain unclear. The present study aimed to investigate the effects of AS‑IV on proliferation and apoptosis of pituitary tumor cells and to elucidate its molecular mechanisms. Cell Counting Kit‑8 (CCK‑8), TUNEL, EdU, immunohistochemistry (IHC), and Western blotting, among others, showed that AS‑IV significantly suppressed the viability of the rat pituitary tumor cell lines GH3 and MMQ in a concentration‑ and time‑dependent manner while inducing apoptosis. Tubulin β4B Class IVb (TUBB4B) was highly expressed in pituitary tumor tissue and its overexpression promoted cell proliferation while inhibiting apoptosis. AS‑IV bound TUBB4B with high affinity, forming a stable complex. TUBB4B regulation influenced pituitary tumor cell sensitivity to AS‑IV, with AS‑IV demonstrating enhanced antitumor efficacy in TUBB4B‑overexpressing tumors. TUBB4B activated the ERK/MAPK signaling pathway by upregulating Stathmin 1 (STMN1) expression, which promoted G1/S phase transition. The ERK‑specific inhibitor U0126 reversed this pro-proliferative effect. To the best of our knowledge, the present study is the first to reveal that AS‑IV inhibits pituitary tumor proliferation and promotes apoptosis by targeting TUBB4B to regulate the STMN1‑ERK signaling axis, providing a novel theoretical basis and potential strategies for traditional Chinese medicine treatment and molecular targeted research on pituitary tumors.
Crosstalk between autophagy and ferroptosis in liver diseases (Review).
Wei Y, Zhou K, Su Y … +7 more , Luan Z, Li P, Chang Y, Han B, Li H, Qiao Y, Ren J
Int J Mol Med · 2026 Jun · PMID 41891979 · Full text
Ferroptosis is a novel form of regulated cell death triggered by iron‑dependent accumulation in lipid peroxidation. Multiple intracellular catabolic processes and signaling pathways are implicated in ferroptosis regulati...
Ferroptosis is a novel form of regulated cell death triggered by iron‑dependent accumulation in lipid peroxidation. Multiple intracellular catabolic processes and signaling pathways are implicated in ferroptosis regulation. One is autophagy, which delivers cytoplasmic materials to lysosomes for degradation and is critical for the preservation of cellular homeostasis. The discovered role of autophagy in driving ferroptosis have motivated further explorations of the functional interactions and signal pathways between ferroptosis and autophagy, particularly their crosstalk in the pathogenesis or treatment for various liver diseases, such as drug‑induced liver injury, toxin‑induced liver injury, liver fibrosis and hepatocellular carcinoma. The present review presented an in‑depth overview of research on the crosstalk between autophagy and ferroptosis in diverse liver diseases, including the ones aforementioned. The diverse regulatory mechanisms involved in this process are also analyzed to open a new perspective on the interpretation of liver diseases manifestations and provide potential targets for drug discovery and effective intervene.
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