Zhou Y, Chen Y, Cui Y
… +8 more, Gan N, Xiang Q, Li M, Zeng W, Zheng XL, Dai X, Peng J, Tang Z
J Cardiovasc Transl Res
· 2025 Aug · PMID 40259193
·
Publisher ↗
Ferroptosis plays a key role in abdominal aortic aneurysm (AAA) development. This study explores whether and how ferroptosis regulates AAA progression. Ferroptosis was confirmed in human AAA tissue. In vitro experiments...Ferroptosis plays a key role in abdominal aortic aneurysm (AAA) development. This study explores whether and how ferroptosis regulates AAA progression. Ferroptosis was confirmed in human AAA tissue. In vitro experiments with primary mouse vascular smooth muscle cells (VSMCs) and abdominal aortic rings revealed that angiotensin II (Ang II) triggered ferroptosis in VSMCs. Ferrostatin-1 (Fer-1), a potent ferroptosis inhibitor, effectively suppressed this effect. Additionally, the ferroptosis inducer erastin and Ang II can both promoted pathological remodeling of abdominal aortic rings, but Fer-1 significantly suppressed these effects. In AAA mouse model, Fer-1 treatment reduced AAA formation. Mechanistically, RNA-sequencing analysis revealed that Fer-1 regulates VSMC contractile function, suppresses inflammation, and mitigates extracellular matrix remodeling. These findings highlight the critical role of VSMC ferroptosis in AAA pathogenesis and demonstrate that ferroptosis inhibition effectively reduces pathological vascular remodeling, making it a promising therapeutic strategy for preventing AAA.
Wang T, Su Z, Zhong M
… +6 more, Wu X, Li L, Gu H, Sun Y, Ji J, Peng X
J Cardiovasc Transl Res
· 2025 Aug · PMID 40237961
·
Publisher ↗
Oxidative stress and protein nonenzymatic glycation are key factors in diabetic-foot syndrome pathogenesis. Type 2 diabetes (T2DM) progression involves excessive gluconolactone (GDL) production, linked to endothelial inj...Oxidative stress and protein nonenzymatic glycation are key factors in diabetic-foot syndrome pathogenesis. Type 2 diabetes (T2DM) progression involves excessive gluconolactone (GDL) production, linked to endothelial injury and diabetic arteriosclerosis. This study explored GDL's role in diabetic-foot syndrome using high-performance liquid chromatography-tandem mass spectrometry to analyze sera from 75 T2DM patients (including 32 with diabetic-foot) and 36 healthy controls. GDL levels were significantly higher in T2DM patients and correlated with increased hemoglobin A1c glycation and reactive oxygen species production in endothelial cells, suggesting GDL's role in accelerating macrovascular arteriosclerosis and diabetic-foot syndrome. These findings highlight GDL's potential as a diagnostic biomarker and therapeutic target for diabetic macrovascular complications.
J Cardiovasc Transl Res
· 2025 Jun · PMID 40229625
·
Full text
Hypertrophic cardiomyopathy (HCM) is the most common genetic myocardial disease, characterized by asymmetric left ventricular hypertrophy (LVH) due to sarcomeric mutations. Aortic stenosis (AS) results in concentric LVH,...Hypertrophic cardiomyopathy (HCM) is the most common genetic myocardial disease, characterized by asymmetric left ventricular hypertrophy (LVH) due to sarcomeric mutations. Aortic stenosis (AS) results in concentric LVH, due to pressure overload. The aim of this study was to identify signaling pathways differentially regulated in HCM compared to AS, using plasma proteomic profiling. 76 HCM cases and 36 AS controls were matched by age and sex. A machine-learning (ML) model to predict HCM was built in the training set (70% cohort) and examined in the test set (30% cohort). Pathway analysis of proteins differentially expressed between HCM and AS was performed. The ML model accurately distinguished HCM from AS, with area under the receiver operating characteristic curve of 0.90 (95% CI: 0.79-1.00). Pathway analysis revealed differential regulation of Ras-MAPK, inflammatory and metabolic pathways. In conclusion, this study identified distinctive proteomic profiles and signaling pathways underlying LVH in HCM compared to AS.
J Cardiovasc Transl Res
· 2025 Aug · PMID 40229624
·
Full text
Stress granules (SGs) are membrane-less cytoplasmic assemblies composed of mRNAs and RNA-binding proteins (RBPs) that transiently form to cope with various cellular stressors by halting mRNA translation and, consequently...Stress granules (SGs) are membrane-less cytoplasmic assemblies composed of mRNAs and RNA-binding proteins (RBPs) that transiently form to cope with various cellular stressors by halting mRNA translation and, consequently, protein synthesis. SG formation plays a crucial role in regulating multiple cellular processes, including cellular senescence, inflammatory responses, and adaptation to oxidative stress under both physiological and pathological conditions. Dysregulation of SG assembly and disassembly has been implicated in the pathogenesis of various diseases, including cardiovascular diseases (CVDs), cancer, viral and bacterial infections, and degenerative diseases. In this review, we survey the key aspects of SGs biogenesis and biological functions, with a particular focus on their causal involvement in CVDs. Furthermore, we summarized several SG-modulating compounds and discussed the therapeutic potential of small molecules targeting SG-related diseases in clinical settings.
Tang H, Kan C, Zhang K
… +7 more, Sheng S, Qiu H, Ma Y, Wang Y, Hou N, Zhang J, Sun X
J Cardiovasc Transl Res
· 2025 Aug · PMID 40227543
·
Publisher ↗
Cardiovascular disease remains a leading cause of mortality worldwide, driven by factors such as dysregulated lipid metabolism, oxidative stress, and inflammation. Recent studies highlight the critical roles of both glyc...Cardiovascular disease remains a leading cause of mortality worldwide, driven by factors such as dysregulated lipid metabolism, oxidative stress, and inflammation. Recent studies highlight the critical roles of both glycerophospholipid and sphingosine- 1-phosphate metabolism in the pathogenesis of cardiovascular disorders. However, the contributions of glycerophospholipid-derived metabolites remain underappreciated. Glycerophospholipid metabolism generates bioactive molecules that contribute to endothelial dysfunction, lipid accumulation, and cardiac cell injury while also modulating inflammatory and oxidative stress responses. Meanwhile, sphingosine- 1-phosphate is a bioactive lipid mediator that regulates vascular integrity, inflammation, and cardiac remodeling through its G-protein-coupled receptors. The convergence of these pathways presents novel therapeutic opportunities, where dietary interventions such as omega- 3 polyunsaturated fatty acids and pharmacological targeting of sphingosine- 1-phosphate receptors could synergistically mitigate cardiovascular risk. This review underscores the need for further investigation into the interplay between glycerophospholipid metabolism and sphingosine- 1-phosphate signaling to advance targeted therapies for the prevention and management of cardiovascular disease.
Wang W, Xu D, Ding J
… +6 more, Pan Y, Wang F, Su S, Peng X, Zhang S, Zhang W
J Cardiovasc Transl Res
· 2025 Jun · PMID 40205317
·
Publisher ↗
Myocardial infarction (MI) is a global health concern that necessitates continued advancements in diagnostic and therapeutic modalities. Nanotechnology facilitates prompt diagnosis and personalized treatment. This manusc...Myocardial infarction (MI) is a global health concern that necessitates continued advancements in diagnostic and therapeutic modalities. Nanotechnology facilitates prompt diagnosis and personalized treatment. This manuscript explicitly reviews the application of innovative methodologies for identifying cardiac biomarkers to facilitate the early diagnosis of MI and its clinical management. Nanoscale agents such as nanoparticles and nanosensors have been employed for this purpose. Technological advancements in medical imaging are revolutionizing therapeutic approaches while reducing morbidity and mortality typically associated with cardiac tissue injury. Besides all, applications of nanotechnology in therapeutics have proven extremely effective. The development of nanoparticle-based customized drug delivery systems will contribute to more effective treatments, fewer side effects, and improved therapeutic outcomes. Biomaterials and nanoscale surgical technologies may benefit patients with MI by promoting tissue regeneration and repair. This manuscript also investigates the ethical and legal limitations that could prevent seamless incorporation of nanotechnology into clinical practice.
Davari M, Khansari M, Hosseini S
… +11 more, Morovatshoar R, Azani A, Mirzohreh ST, Mahabadi MA, Ghasemi M, Meigoli MSS, Nematollahi SF, Pourranjbar S, Behfar Q, Baghdadi M, Hosseini AM
J Cardiovasc Transl Res
· 2025 Dec · PMID 40198537
·
Publisher ↗
Myocardial ischemia-reperfusion injury (IRI) is a major issue in cardiovascular medicine, marked by tissue damage from the restoration of blood flow after ischemia. Opioids, known for their pain-relieving properties, hav...Myocardial ischemia-reperfusion injury (IRI) is a major issue in cardiovascular medicine, marked by tissue damage from the restoration of blood flow after ischemia. Opioids, known for their pain-relieving properties, have emerged as potential cardioprotective agents in IRI. Recent research suggests opioids influence epigenetic mechanisms-such as histone modifications and non-coding RNAs (ncRNAs)-which are essential for regulating gene expression and cellular responses during myocardial IRI. This review delves into how opioids like remifentanil affect histone modifications, DNA methylation, and ncRNAs, including microRNAs (miRNAs) and long non-coding RNAs (lncRNAs). Remifentanil postconditioning (RPC) reduces apoptosis in cardiomyocytes through histone deacetylation, specifically downregulating histone deacetylase 3 (HDAC3). Similarly, opioids impact miRNAs such as miR- 206 - 3p and miR- 320 - 3p, and lncRNAs like TINCR and UCA1, which influence apoptosis, inflammation, and oxidative stress. Understanding these interactions highlights the potential for opioid-based therapies in mitigating IRI-induced myocardial damage.
J Cardiovasc Transl Res
· 2025 Jun · PMID 40195213
·
Publisher ↗
The magnesium depletion score (MDS) is considered a new valuable predictor of body magnesium status. This study aimed to explore the association between MDS and PAD among participants aged ≥ 40 years on the National Heal...The magnesium depletion score (MDS) is considered a new valuable predictor of body magnesium status. This study aimed to explore the association between MDS and PAD among participants aged ≥ 40 years on the National Health and Nutrition Examination Survey in 1999-2004. Survey-weighted multivariable logistic regression and restricted cubic spline models were used to assess the association between MDS and PAD. Survey-weighted multivariable logistic regression showed a significant positive association between MDS and the prevalence of PAD. For each unit increase in MDS, the risk of PAD increased by 24%. Compared to individuals with MDS = 0, those with MDS ≥ 3 had a 95% higher risk of PAD. Restricted triple spline analysis showed a linear dose-response relationship between MDS and PAD risk. Subgroup analysis indicated that this positive association was stronger in individuals aged > 60 years. Numerous future longitudinal cohort studies are required to validate our findings.
Xiang L, Yin G, Gong Z
… +11 more, Lv X, Feng C, Liu L, Abdu FA, Shi T, Zhang W, Alifu J, Xu X, Dai Y, Che W, Weng X
J Cardiovasc Transl Res
· 2025 Jun · PMID 40195212
·
Publisher ↗
Heart failure (HF) due to left ventricular (LV) dysfunction remains a major global health challenge, with inflammation driving its progression under chronic pressure overload, such as hypertension. This study explored th...Heart failure (HF) due to left ventricular (LV) dysfunction remains a major global health challenge, with inflammation driving its progression under chronic pressure overload, such as hypertension. This study explored the role of interleukin-22 (IL-22), a cytokine associated with tissue protection, in HF induced by transverse aortic constriction (TAC). IL-22 knockout (KO) mice exhibited exacerbated HF, marked by worsened LV hypertrophy, heightened inflammation, and impaired cardiac function compared to wild-type controls. Conversely, treatment with recombinant IL-22Fc improved LV function, reduced inflammatory cell infiltration, and alleviated cardiac remodeling and inflammation. These findings demonstrate that IL-22 plays a critical role in regulating inflammation and cardiac remodeling in pressure overload-induced HF. Targeting IL-22 may represent a promising therapeutic strategy to alleviate HF progression and associated pulmonary complications.
J Cardiovasc Transl Res
· 2025 Aug · PMID 40167980
·
Publisher ↗
Pulmonary arterial hypertension (PAH) poses a challenge due to limited curative options and ineffective treatments. Mesenchymal stem cell (MSC) therapy has emerged as a potential intervention for PAH. This study delved i...Pulmonary arterial hypertension (PAH) poses a challenge due to limited curative options and ineffective treatments. Mesenchymal stem cell (MSC) therapy has emerged as a potential intervention for PAH. This study delved into the therapeutic potential and molecular mechanisms underlying MSC-based apelin gene therapy in PAH rats induced by monocrotaline (MCT). Wharton's jelly-derived MSCs transfected with pcSLenti-APLN were utilized as therapeutic agents. Transplanted MSCs successfully homed to the lung tissue of rats and sustained survival for at least three weeks. MSC-mediated apelin gene therapy effectively reduced pulmonary artery pressure, mitigated pulmonary vascular remodeling, and modulated apoptosis in MCT-induced PAH rats. Furthermore, the phosphatidylinositol 3-kinase (PI3K)/AKT/endothelial nitric oxide synthase (eNOS) and ERK1/2 signaling pathways were involved in the therapeutic effects. Meanwhile, Apelin-MSCs also regulated MCT-induced changes of Bax and Bcl-2 in the lung lobes and pulmonary arterioles. MSC-based apelin gene therapy could be considered a possible therapeutic strategy for PAH.
J Cardiovasc Transl Res
· 2025 Jun · PMID 40140177
·
Publisher ↗
Heart failure (HF) treatment remains one of the major challenges in cardiovascular disease management, and its pathogenesis requires further exploration. Cardiac metabolic remodeling is of great significance as a key pat...Heart failure (HF) treatment remains one of the major challenges in cardiovascular disease management, and its pathogenesis requires further exploration. Cardiac metabolic remodeling is of great significance as a key pathological process in the progression of HF. The complex alterations of metabolic substrates and associated enzymes in mitochondria create a vicious cycle in HF. These changes lead to increased reactive oxygen species, altered mitochondrial Ca handling, and the accumulation of fatty acids, contributing to impaired mitochondrial function. In this context, mitophagy plays a significant role in clearing damaged mitochondria, thereby maintaining mitochondrial function and preserving cardiac function by modulating metabolic remodeling in HF. This article aims to explore the role of mitophagy in cardiac metabolic remodeling in HF, especially in obesity cardiomyopathy, diabetic cardiomyopathy, and excessive afterload-induced heart failure, thoroughly analyze its molecular mechanisms, and review the therapeutic strategies and prospects based on the regulation of mitophagy.
J Cardiovasc Transl Res
· 2025 Jun · PMID 40133736
·
Full text
Lipoxygenases (LOXs) are a family of dioxygenases that catalyze the peroxidation of polyunsaturated fatty acids, such as linoleic acid and arachidonic acid, initiating the synthesis of bioactive lipid mediators. The LOX-...Lipoxygenases (LOXs) are a family of dioxygenases that catalyze the peroxidation of polyunsaturated fatty acids, such as linoleic acid and arachidonic acid, initiating the synthesis of bioactive lipid mediators. The LOX-mediated production of these bioactive molecules in various cell types plays a critical role in the pathophysiology of cardiovascular diseases, including atherosclerosis, hypertension, and myocardial ischemia-reperfusion injury. In this review, we summarize the roles of LOXs and their products in different cardiovascular cells and conditions, offering valuable insights may contribute to the development of novel therapeutic strategies for cardiovascular diseases.
J Cardiovasc Transl Res
· 2025 Jun · PMID 40131655
·
Full text
Translational models for obstructive coronary artery disease are lacking. We aimed to develop a porcine model for obstructive coronary stenosis induced by bioresorbable stent (BRS) implantation in hypercholesterolemic pr...Translational models for obstructive coronary artery disease are lacking. We aimed to develop a porcine model for obstructive coronary stenosis induced by bioresorbable stent (BRS) implantation in hypercholesterolemic proprotein convertase subtilisin/kexin-9 (PCSK9) minipigs. Fifteen hypercholesterolemic PCSK9 minipigs were randomized to percutaneous coronary intervention with Magmaris, Absorb or Desolve BRS. Optical coherence tomography (OCT) scans were performed at baseline and 6-months followed by histology. Matched OCT analysis showed minimal lumen area decreased from 7.62 ± 1.54 mm at baseline to 2.12 ± 0.92 mm at follow-up in the Magmaris group, from 6.99 ± 1.49 mm to 3.07 ± 1.52 mm in the Absorb group, and from 6.05 ± 1.11 mm to 2.65 ± 0.93 mm in the Desolve group. Histologic examination revealed advanced human-like stenosis. BRS implantation in hypercholesterolemic PCSK9 minipigs induced human-like stenoses and may serve as a feasible preclinical model for obstructive coronary artery disease.
Ding J, Yang A, Zhou L
… +8 more, Zhang F, Zhou H, Zhang Y, Wang Y, Liu Y, Liang D, Liu Y, Wu Y
J Cardiovasc Transl Res
· 2025 Jun · PMID 40095199
·
Publisher ↗
Cardiomyocyte hypertrophy is a key remodeling response to cardiac stress and an independent risk factor for heart failure. However, the molecular mechanism of cardiomyocyte hypertrophy is not yet fully understood. We her...Cardiomyocyte hypertrophy is a key remodeling response to cardiac stress and an independent risk factor for heart failure. However, the molecular mechanism of cardiomyocyte hypertrophy is not yet fully understood. We here found Polo-like kinase 1 (PLK1) was crucial in regulating endothelin-1 (ET-1)-induced cardiomyocyte hypertrophy. Notably, PLK1 expression was significantly elevated in ET-1-induced hypertrophic cardiomyocytes and pressure overload-induced hypertrophic cardiac tissue. Knocking down Plk1 reduced the cell size of hypertrophic cardiomyocytes and suppressed the expression of hypertrophic markers, including ANP, BNP and β-MHC. The PLK1 inhibitor BI2536 had similar effects on hypertrophic cardiomyocytes. Mechanistically, the ERK1/2 pathway was identified as the key downstream pathway mediating the effects of PLK1 on ET-1-induced cardiomyocyte hypertrophy. Finally, the deficiency of PLK1 attenuated the hypertrophy of hiPSC-CMs. In summary, our study revealed that PLK1 regulates ET-1-induced cardiomyocyte hypertrophy through the ERK1/2 pathway, providing insights into the pathogenesis and potential therapies for pathological cardiac hypertrophy.
Hou X, Hu G, Wang H
… +3 more, Yang Y, Sun Q, Bai X
J Cardiovasc Transl Res
· 2025 Jun · PMID 40095198
·
Publisher ↗
Heart failure (HF) is a clinical syndrome caused by structural or functional abnormalities in heart. Egr2 has been reported to be protective for multiple diseases, but its effect on HF remains unknown. The present study...Heart failure (HF) is a clinical syndrome caused by structural or functional abnormalities in heart. Egr2 has been reported to be protective for multiple diseases, but its effect on HF remains unknown. The present study intended to investigate the potential role of Egr2 in HF and its possible downstream effectors. High Egr2 expression in heart was observed in HF mice. Egr2 knockdown alleviated cardiac damage and function in HF mice. Egr2 knockdown inhibited myocardial inflammation and apoptosis both in vivo and in vitro. Egr2 inhibited Acot1 transcription expression via directly binding to its promoter. Acot1 overexpression reduced Lipopolysaccharide (LPS)-induced cardiomyocyte inflammation and apoptosis. Functional rescue experiments revealed that Acot1 reversed the effects of Egr2 on LPS-induced cell apoptosis and inflammation. Overall, Egr2 knockdown might ameliorate HF by inhibiting inflammation and apoptosis in cardiomyocytes by targeting Acot1. This study might provide evidence to better understand the molecular mechanisms of HF pathogenesis.
Demkes E, Cervera-Barea A, Ebner-Peking P
… +20 more, Wolf M, Hochmann S, Scheren AS, Bijsterveld M, van Oostveen CM, Jansen M, Visser J, Triebert W, Halloin C, Dobbe JGG, de Vos J, Schürz M, Danmayr J, Aalders MCG, Boink GJJ, Neef K, Strunk D, Zweigerdt R, de Jager SCA, Sluijter JPG
J Cardiovasc Transl Res
· 2025 Jun · PMID 40082315
·
Full text
Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) constitute a promising therapy for myocardial infarction (MI). The lack of an effective immunosuppressive regimen, combined with single-cell transpla...Human-induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) constitute a promising therapy for myocardial infarction (MI). The lack of an effective immunosuppressive regimen, combined with single-cell transplantations, results in suboptimal outcomes, such as poor engraftment and compromised therapeutic efficacy. This study aimed to confirm the increased retention of hiPSC-CMs microtissues (CMTs) over single-cell grafts. To ensure the long-term survival of CMTs for potential cardiac applications, CMTs were transplanted in a porcine model of MI using a triple immunosuppression protocol designed to limit immune cell infiltration. Acute evaluation of spherical hiPSC-CMs aggregates and dissociated aggregates followed by the development of a triple immunosuppression protocol were performed in healthy animals. Long-term survival of CMTs was later examined in pigs that underwent a transient coronary occlusion. Two weeks post-MI, the immunosuppression treatment was initiated and on day 28 the animals were transplanted with CMTs and followed for four more weeks. Acutely, CMTs showed superior retention compared to their dissociated counterparts. The immunosuppression regimen led to no organ damage and stable levels of circulating drugs once optimal dose was achieved. Two weeks post-xenotransplantation in healthy pigs, histology revealed that immunosuppressed animals displayed a significant decrease in total cellular infiltrates, particularly in CD3 T cells. Pigs that underwent coronary occlusion, which later were immunosuppressed and treated with CMTs (5 × 10 cells), showed cell engraftment onto the native myocardium four weeks post-transplantation. This study supports the use of a triple immunosuppression cocktail to ensure long-term survival of CMTs for the treatment of MI.
Mohammadi A, Karimian A, Shokri K
… +6 more, Mohammadi A, Hazhir-Karzar N, Bahar R, Radfar A, Pakyari M, Tehrani B
J Cardiovasc Transl Res
· 2025 Aug · PMID 40080261
·
Publisher ↗
Cardio-Kidney-Metabolic (CKM) Syndrome involves metabolic, kidney, and cardiovascular dysfunction, disproportionately affecting disadvantaged groups. Its staging (0-4) highlights the importance of early intervention. Whi...Cardio-Kidney-Metabolic (CKM) Syndrome involves metabolic, kidney, and cardiovascular dysfunction, disproportionately affecting disadvantaged groups. Its staging (0-4) highlights the importance of early intervention. While current management targets hypertension, heart failure, dyslipidemia, and diabetes, RNA-based therapies offer innovative solutions by addressing molecular mechanisms of CKM Syndrome. Emerging RNA treatments, including antisense oligonucleotides (ASOs) and small interfering RNAs (siRNAs), show promise in slowing disease progression across CKM stages. For example, ASOs and siRNAs targeting ApoC-III and ANGPTL3 reduce triglycerides and LDL cholesterol, while siRNAs improve blood pressure control by targeting the renin-angiotensin-aldosterone system. Obesity treatments leveraging miRNAs and circRNAs tackle a key CKM risk factor. In heart failure and diabetes, RNA-based therapies improve cardiac function and glucose control, while early kidney disease trials show potential for RNAi in acute injury. Further research is essential to refine these therapies and ensure equitable access.
Qin HD, Yang Y, Xie F
… +5 more, Hou L, Gao H, Tang JW, Shao XS, Qin CC
J Cardiovasc Transl Res
· 2025 Jun · PMID 40072709
·
Full text
Acute postinfarction ventricular septum defect has a persistently high mortality rate due to unstable scars in the acute phase, which make surgery or occluder use unsuitable. Delayed closure increases the risk of irrever...Acute postinfarction ventricular septum defect has a persistently high mortality rate due to unstable scars in the acute phase, which make surgery or occluder use unsuitable. Delayed closure increases the risk of irreversible hemodynamic deterioration. To address this, a dual latex balloon catheter was designed for temporary closure and tested in a pig model. The catheter, with a 10 French profile and 80 cm in length, includes two independent latex balloons and an anticoagulant channel to prevent thrombus formation. It was inserted via the jugular vein and guided over a 0.014-inch wire to straddle and seal the ventricular septum defect. In eight Yorkshire pigs with ventricular septum defects and acute myocardial infarction, the catheter effectively closed defects ranging from 6.1 to 10.5 mm for two weeks without complications. This innovative tool shows promise as a bridge therapy for managing acute postinfarction ventricular septum defect and warrants further evaluation.
Fang J, Wu S, Zhao H
… +5 more, Zhou C, Xue L, Lei Z, Li H, Shan Z
J Cardiovasc Transl Res
· 2025 Jun · PMID 40032789
·
Full text
Post-translational modifications (PTMs), which are covalent alterations of proteins after their synthesis, are critical for their proper function and the maintenance of cellular physiology. The significance of PTMs in th...Post-translational modifications (PTMs), which are covalent alterations of proteins after their synthesis, are critical for their proper function and the maintenance of cellular physiology. The significance of PTMs in the context of cardiovascular diseases (CVDs) has been increasingly recognized due to their potential to influence protein stability, activity, and localization, thereby affecting the progression of CVDs. The identification and understanding of PTMs in CVDs at the molecular level are vital for the discovery of new biomarkers and new targets for clinical interventions. This article provides a comprehensive overview of the role and mechanisms of new types of PTMs, such as acetylation, crotonylation, succinylation, S-nitrosylation, malonylation, S-palmitonylation, β-hydroxybutyrylation and lactylation, in CVDs, highlighting their importance in advancing diagnostic and therapeutic approaches for CVDs.
J Cardiovasc Transl Res
· 2025 Jun · PMID 39971891
·
Full text
Coarctation of the aorta (CoA) can cause aortic obstruction, ischemia, and death. Resonance Raman Spectroscopy (RRS) measures tissue oxyhemoglobin (ShbO) and mitochondrial redox state (3RMR) non-invasively. Metal wire wa...Coarctation of the aorta (CoA) can cause aortic obstruction, ischemia, and death. Resonance Raman Spectroscopy (RRS) measures tissue oxyhemoglobin (ShbO) and mitochondrial redox state (3RMR) non-invasively. Metal wire was placed around the aorta of Sprague Dawley rats to generate a systolic blood pressure (SBP) gradient. RRS-ShbO and 3RMR were measured pre- (hand) and post-obstruction (foot). In model 1 (n = 8), the gradient rapidly reached 120 mmHg. In model 2 (n = 30), gradients of 20 mmHg (n = 9) and 40 mmHg (n = 12) were maintained for 2 h. In model 1, foot-ShbO and 3RMR changed significantly (P = 0.004 and P = 0.007) at SBP gradients of 80-mmHg or above. In model 2, the 40-mmHg gradient group showed significant declines in foot-ShbO2 (P = 0.014) and increases in 3RMR (P = 0.008) by 1 h. Foot-ShbO and 3RMR correlated strongly with serum mixed venous saturation (ShbO: r = 0.73, P < 0.0001; 3RMR: r = -0.55, P < 0.0001). RRS effectively detects ischemia caused by aortic obstruction in a CoA model.