Journal of Cardiovascular Pharmacology最新文献_第5页

Flavin Adenine Dinucleotide Ameliorates Pressure Overload-Induced Heart Failure by Activating the Short-Chain Acyl-CoA Dehydrogenase. 黄素腺嘌呤二核苷酸通过激活短链酰基辅酶a脱氢酶改善压力过载引起的心力衰竭。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-06-19 eCollection Date: 2025-07-01 DOI: 10.1097/FJC.0000000000001698

Chunyu Chen, Xue Qin, Yuhong Cao, Liyuan Qing, Zhichao Ma, Qingping Xu, Huan Peng, Guifang Jin, Zhicheng Yang, Jieyu Xing, Sigui Zhou

{"title":"Flavin Adenine Dinucleotide Ameliorates Pressure Overload-Induced Heart Failure by Activating the Short-Chain Acyl-CoA Dehydrogenase.","authors":"Chunyu Chen, Xue Qin, Yuhong Cao, Liyuan Qing, Zhichao Ma, Qingping Xu, Huan Peng, Guifang Jin, Zhicheng Yang, Jieyu Xing, Sigui Zhou","doi":"10.1097/FJC.0000000000001698","DOIUrl":"10.1097/FJC.0000000000001698","url":null,"abstract":"Abstract: Flavin adenine dinucleotide (FAD), a cofactor that catalyzes the reaction of flavin protein, participates in fatty acid β-oxidation, which has been shown to inhibit pathological cardiac hypertrophy and fibrosis in spontaneously hypertensive rats. However, the therapeutic advantage of FAD for heart failure (HF) treatment has not been investigated. This study aimed to explore the effects and underlying mechanisms of FAD in a transverse aortic constriction-induced HF mouse model and in vitro tert-butyl hydroperoxide (tBHP)-induced cardiomyocyte apoptosis model experiments. FAD considerably inhibited tBHP-induced cardiomyocyte apoptosis. In addition, FAD significantly increased the activity and expression of the short-chain acyl-CoA dehydrogenase enzyme and adenosine triphosphate (ATP) content while reducing the content of free fatty acids and reactive oxygen species both in vitro and in vivo. Meanwhile, FAD increased the mitochondrial membrane potential, suppressed mitochondrial membrane swelling, and decreased myocardial fibrosis and TUNEL-positive apoptosis cells in the TAC-induced HF mice. In conclusion, our results indicate that FAD plays a positive role in preventing and treating HF, which can be attributed in part to the activation of short-chain acyl-CoA dehydrogenase.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"84-96"},"PeriodicalIF":2.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143811523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of Muscarinic Acetylcholine Receptors in Oxytocin-Induced Cardioprotection Against Ischemia-Reperfusion Injury in Rats. 毒蕈碱类乙酰胆碱受体在催产素诱导大鼠心肌缺血再灌注损伤中的作用。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-06-19 eCollection Date: 2025-07-01 DOI: 10.1097/FJC.0000000000001701

Mahdieh Faghihi, Mohammadreza Ahmadi-Beni, Fariba Houshmand

{"title":"Role of Muscarinic Acetylcholine Receptors in Oxytocin-Induced Cardioprotection Against Ischemia-Reperfusion Injury in Rats.","authors":"Mahdieh Faghihi, Mohammadreza Ahmadi-Beni, Fariba Houshmand","doi":"10.1097/FJC.0000000000001701","DOIUrl":"10.1097/FJC.0000000000001701","url":null,"abstract":"Abstract: Oxytocin (OT) has been shown to provide myocardial protection against ischemia-reperfusion (I/R) injury. This study investigates the involvement of muscarinic receptors in the OT-induced cardioprotection, focusing on its potential mechanisms and effects on myocardial infarction (MI) and ischemic arrhythmias. Male rats anesthetized with pentobarbital sodium were subjected to 25-minute ischemia followed by 120-minute reperfusion after intraperitoneal administration of OT (0.01 μg), atropine (1.5 µg/kg), or saline. Cardioprotection was evaluated by monitoring lactate dehydrogenase, malondialdehyde, and cardiac creatine kinase isoenzyme levels, infarct size, arrhythmia severity, ventricular fibrillation (VF), and mortality. OT markedly reduced infarct size, oxidative stress, and the severity of ischemic arrhythmias, including ventricular tachycardia and VF, compared with saline-treated I/R animals. OT also significantly improved survival rates. Pretreatment with atropine abolished most protective effects of OT but did not significantly alter its suppression of VF, suggesting the involvement of muscarinic receptor-independent mechanisms. These findings highlight that the OT-induced cardioprotection, mediated in part by acetylcholine locally released in the left ventricle, extends beyond infarct limitation to include potent antiarrhythmic effects. The dual impact of OT on MI and arrhythmias provides insights into the mechanisms underlying its preconditioning effect and its potential application in MI management.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":"109-117"},"PeriodicalIF":2.6,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144025552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

miR-132 inhibition improves cardiac remodeling and function in a two-hit mouse model of heart failure with a preserved ejection fraction. 在保留射血分数的心力衰竭小鼠模型中，miR-132抑制可改善心脏重塑和功能。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-06-18 DOI: 10.1097/FJC.0000000000001729

Ying Wu, Meiyan Song, Wen Chen, Fengjin Liang, Kaizu Xu, Liming Lin, Meifang Wu

{"title":"miR-132 inhibition improves cardiac remodeling and function in a two-hit mouse model of heart failure with a preserved ejection fraction.","authors":"Ying Wu, Meiyan Song, Wen Chen, Fengjin Liang, Kaizu Xu, Liming Lin, Meifang Wu","doi":"10.1097/FJC.0000000000001729","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001729","url":null,"abstract":"To investigate the impact of antimiR-132, a miR-132 antisense inhibitor, on cardiac remodeling and function in a two-hit mouse model of heart failure with preserved ejection fraction (HFpEF), as well as its underlying mechanism. Male C57BL/6 mice were fed N(omega)-nitro-L-arginine methyl ester plus a high-fat diet to establish an HFpEF model, and then intraperitoneally injected with antimiR-132 or normal saline. Cardiac fibroblasts treated with transforming growth factor β1 (TGF-β1) were cultured in the presence of antimiR-132 or vehicle to examine collagen synthesis and potential mechanisms. Compared to control mice, HFpEF mice showed significant increases in blood pressure, triglycerides, cholesterol, body weight, myocardial hypertrophy, and fibrosis. They also had elevated E/E' ratios and plasma NT-proBNP levels. antimiR-132 did not significantly impact blood pressure or metabolic parameters in HFpEF mice; however, it notably ameliorated myocardial hypertrophy and fibrosis, while concurrently reducing E/E' ratios and plasma NT-proBNP levels. Mechanistically, the cardioprotective effects of antimiR-132 were accompanied by inhibition of the upregulated expression of miR-132 and P-Smad3 protein in the myocardium, as well as reduction in TGF-β1-induced collagen synthesis and Smad3 phosphorylation in cardiac fibroblasts. Taken together, miR-132 inhibition ameliorated myocardial remodeling and diastolic dysfunction in HFpEF mice through downregulation of the miR-132/Smad3 pathway.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325879","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Types, Molecular Mechanisms and Potential Therapeutic Targets of Programmed Endothelial Cell Death in Atherosclerosis. 动脉粥样硬化中程序性内皮细胞死亡的类型、分子机制和潜在治疗靶点。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-06-18 DOI: 10.1097/FJC.0000000000001728

Lu Kuang, Qijun Chen, Zenghui Liu, Limei Wu, Shaoguo Wu

引用次数: 0

Methotrexate improves left ventricle systolic and diastolic function in induced Takotsubo myocardiopathy rats. 甲氨蝶呤改善Takotsubo型心肌病大鼠左心室收缩和舒张功能。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-06-18 DOI: 10.1097/FJC.0000000000001730

Maria Carolina Guido, Lucas Lage Marinho, Elaine Rufo Tavares, Natalia de Menezes Lopes, Déborah Lima Bispo, Marcelo Dantas Tavares de Melo, Fabiana Hanna Rached, Vera Maria Cury Salemi, Raul Cavalcante Maranhão

{"title":"Methotrexate improves left ventricle systolic and diastolic function in induced Takotsubo myocardiopathy rats.","authors":"Maria Carolina Guido, Lucas Lage Marinho, Elaine Rufo Tavares, Natalia de Menezes Lopes, Déborah Lima Bispo, Marcelo Dantas Tavares de Melo, Fabiana Hanna Rached, Vera Maria Cury Salemi, Raul Cavalcante Maranhão","doi":"10.1097/FJC.0000000000001730","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001730","url":null,"abstract":"Takotsubo syndrome (TTS) is a stress-induced cardiomyopathy which is associated with important morbidity and in-hospital mortality. Microvascular dysfunction, inflammation and fibrosis may play crucial roles in TTS pathophysiology. Here we investigated the effect of methotrexate (MTX), an antiproliferative and immunosuppressive drug, on ventricular function in a rat model of Takotsubo syndrome. TTS induction was performed in Wistar male rats with 2 subcutaneous injections of isoproterenol (ISO, 85mg/Kg), with a 24-hour interval. Twenty-seven animals were allocated to 3 groups: Sham: controls treated with saline solution; ISO: TTS-induced with ISO, treated with saline solution; MTX: TTS-induced with ISO, treated with MTX (1mg/Kg i.p.). Animals were treated once a week, for 4 weeks. After treatments, animals underwent an echocardiographic exam. Histology and protein expression of markers of apoptosis, angiogenesis, and fibrosis were performed. Linear correlation was used to test echocardiographic variables versus protein expression. MTX treatment improved LV the systolic and diastolic functions in TTS rats, shown by higher ejection fraction (66% vs. 44%, p<0.05) and normalized E/A ratio (1.6±0.3 vs. 3.4±0.7, p<0.05). MTX reduced myocardial fibrosis in subendocardium and interstitium and decreased expression of pro-apoptotic markers (caspase 3 and BAX/Bcl-2 ratio). Additionally, MTX-treated rats exhibited reduced hypoxia, as indicated by lower HIF-2α expression, and increased angiogenesis, evidenced by elevated VEGF. In conclusion, MTX treatment enhances cardiac function and decreases adverse remodeling in this TTS rat model, conceivably through anti-fibrotic and pro-angiogenic mechanisms. These findings suggest that MTX may be a promising therapeutic option for TTS, warranting further investigation.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cardiac-specific overexpression of Klotho attenuates paraquat-induced myocardial injury by enhancing the Nrf2/ARE signaling pathway. 心脏特异性过表达Klotho通过增强Nrf2/ARE信号通路减轻百草枯诱导的心肌损伤。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-06-16 DOI: 10.1097/FJC.0000000000001721

Xiao Qian Feng, Ai Ping Deng, Yi Qin Wu, Cheng Zhe Cai, Xian Qu Ye, Ping Fang Liu, Xiang Jin Huang, Zhi Jun Li, Zhuo Fan Xu

{"title":"Cardiac-specific overexpression of Klotho attenuates paraquat-induced myocardial injury by enhancing the Nrf2/ARE signaling pathway.","authors":"Xiao Qian Feng, Ai Ping Deng, Yi Qin Wu, Cheng Zhe Cai, Xian Qu Ye, Ping Fang Liu, Xiang Jin Huang, Zhi Jun Li, Zhuo Fan Xu","doi":"10.1097/FJC.0000000000001721","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001721","url":null,"abstract":"Paraquat, a widely used herbicide, is known to induce oxidative stress and inflammation, which leads to myocardial injury. Klotho, a protein with antioxidative and anti-inflammatory properties, has garnered as a potential cardioprotective factor. This study aimed to investigate whether cardiac-specific overexpression of klotho mitigates paraquat-induced myocardial injury through the activation of the NF-E2-related factor-2 (Nrf-2)/antioxidant response element (ARE) signaling pathway. Our results revealed that both mRNA and protein expressions of Klotho were significantly reduced in the myocardial tissue of paraquat-exposed rats. However, cardiac-specific overexpression of Klotho significantly restored Klotho levels and attenuated paraquat-induced myocardial injury, as evidenced by the decreased lactate dehydrogenase (LDH) and cardiac troponin I (cTnI) contents, and creatine kinase (CK) activity, alongside with apoptosis. Furthermore, cardiac-specific overexpression of Klotho inhibited oxidative stress and inflammation in myocardial tissue of paraquat-subjected rats. Mechanistically, Klotho activated of the Nrf2/ARE signaling pathway, upregulating cytoprotective genes such as NAD(P)H quinone oxidoreductase 1 (NQO1), heme oxygenase-1 (HO-1), glutamate cysteine ligase catalytic (GCLC) subunit, and glutamate cysteine ligase modifier (GCLM) subunit. Our findings indicate that Klotho protects against paraquat-induced myocardial injury by suppressing oxidative stress and inflammation, primarily via the activation of the Nrf2/ARE signaling pathway. These results underscore the potential therapeutic role of Klotho in preventing paraquat-induced myocardial damage.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetic exploration of targeting the transient receptor potential cation channel subfamily member 6. 靶向瞬时受体电位阳离子通道亚家族成员的遗传探索

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-06-11 DOI: 10.1097/FJC.0000000000001727

Christian Graesser, Nikita Panyam, Xiaofeng Qian, Tan An Dang, Benedikt Niedermeier, Michael Winkler, Johannes Riechel, M Amin Sharifi, Christin Noecker, Carla Abrahamian, Alexander Dietrich, Hendrik B Sager, Heribert Schunkert, Ling Li, Thorsten Kessler

{"title":"Genetic exploration of targeting the transient receptor potential cation channel subfamily member 6.","authors":"Christian Graesser, Nikita Panyam, Xiaofeng Qian, Tan An Dang, Benedikt Niedermeier, Michael Winkler, Johannes Riechel, M Amin Sharifi, Christin Noecker, Carla Abrahamian, Alexander Dietrich, Hendrik B Sager, Heribert Schunkert, Ling Li, Thorsten Kessler","doi":"10.1097/FJC.0000000000001727","DOIUrl":"https://doi.org/10.1097/FJC.0000000000001727","url":null,"abstract":"The transient receptor potential cation channel subfamily member 6 (TRPC6) represents an emerging druggable target with a broad therapeutic spectrum. TRPC6 Inhibitors are currently investigated for focal segmental glomerulosclerosis (FSGS), acute respiratory distress syndrome due to COVID-19, and pulmonary hypertension. In the cardiovascular system, there is evidence that TRPC6 is critically involved in the development of cardiac hypertrophy, arrhythmia susceptibility and risk of restenosis after coronary stent implantation. However, data on systemic effects of TRPC6 modulation remain scarce. To assess the phenotypic consequences of inhibiting TRPC6 in different organ systems, we explored public databases to identify single nucleotide polymorphisms (SNPs) that are associated with TRPC6 expression in different tissues. A phenome-wide association study was then performed in 475,739 individuals of UK Biobank to associate genetically-mediated reduced TRPC6 expression with 64 phenotypes in nine organ/disease categories. Lower TRPC6 expression was nominally associated with reduced risk of anxiety, heart failure, and stroke, as well as an increased risk of venous thromboembolism, hypertension, appendicitis and liver cirrhosis. After correction for multiple testing, lower TRPC6 expression remained significantly associated with reduced risk of coronary artery disease and atrial fibrillation. Notably, no deleterious phenotypes were observed, suggesting a favorable profile of systemic TRPC6 inhibition. While these findings indicate potential therapeutic benefits, nominally associated phenotypes, however, mandate careful clinical investigation and provide a basis for further experimental exploration.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.6,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144266328","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differential Binding Affinities and Kinetics of Transthyretin Stabilizers. 转甲状腺素稳定剂的不同结合亲和力和动力学。

IF 2.2 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-06-05 DOI: 10.1097/FJC.0000000000001726

Alan X Ji, Andreas Betz, Uma Sinha

{"title":"Differential Binding Affinities and Kinetics of Transthyretin Stabilizers.","authors":"Alan X Ji, Andreas Betz, Uma Sinha","doi":"10.1097/FJC.0000000000001726","DOIUrl":"10.1097/FJC.0000000000001726","url":null,"abstract":"Transthyretin amyloid cardiomyopathy (ATTR-CM) is a progressive, fatal disease. Dissociation of tetrameric transthyretin (TTR) is the triggering event in the pathogenic mechanism; destabilizing TTR mutations accelerate the process. The TTR stabilizers, tafamidis and acoramidis, are the only FDA approved treatments for patients with ATTR-CM. By mimicking the stabilizing characteristics of the super-stabilizing, disease-protecting variant T119M, we hypothesize that acoramidis displays differential TTR binding, kinetic stability, and tetramer stabilization compared with other TTR stabilizers, such as tafamidis and diflunisal. The TTR binding affinity and thermodynamic stability of TTR interaction of acoramidis and tafamidis were assessed by surface plasmon resonance (SPR) and microscale thermophoresis (MST). Tetrameric TTR stabilization by acoramidis, tafamidis, and diflunisal in the presence of plasma proteins against acidic denaturation was measured by immune blots. In kinetic studies, SPR demonstrated 4 times longer residence time for acoramidis bound to TTR compared with tafamidis. The dissociation constants were consistent with those determined by equilibrium measurements in MST. The affinity of acoramidis for purified TTR, as measured by MST, was 4 times higher than that of tafamidis. When tested at clinically relevant plasma concentrations, acoramidis stabilized TTR against acidic denaturation to a much higher extent (≥90%) than tafamidis or diflunisal. Of note, both tafamidis and diflunisal demonstrated partial stabilization of tetrameric TTR. Relative to other stabilizers, acoramidis is more potent as independently assessed by TTR binding affinity, kinetic stability, and acid-mediated denaturation. These properties may contribute to the ability of acoramidis to achieve near-complete stabilization of TTR in plasma samples.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-06-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12333512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234240","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Metabolic dysregulation of hydrogen sulfide as a driver of vascular disease. 硫化氢代谢失调是血管疾病的驱动因素。

IF 2.6 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-06-04 DOI: 10.1097/FJC.0000000000001725

Alexander E Berezin

引用次数: 0

The therapeutic potential of hydrogen sulfide and its donors, a new discovery in vascular diseases. 硫化氢及其供体的治疗潜力，血管疾病的新发现。

IF 2.2 4区医学

Journal of Cardiovascular Pharmacology Pub Date : 2025-05-30 DOI: 10.1097/FJC.0000000000001714

Youzhen Pu, Wenlong Lin, Suyi Ren, Yuxu Gao, Guiming Wang

{"title":"The therapeutic potential of hydrogen sulfide and its donors, a new discovery in vascular diseases.","authors":"Youzhen Pu, Wenlong Lin, Suyi Ren, Yuxu Gao, Guiming Wang","doi":"10.1097/FJC.0000000000001714","DOIUrl":"10.1097/FJC.0000000000001714","url":null,"abstract":"Abstract: Hydrogen sulfide (H 2 S), an important gaseous signaling molecule, plays a critical role in maintaining vascular homeostasis. H 2 S participates in numerous biological functions, including redox regulation, interactions with other signaling molecules, and post-translational modifications of proteins through sulfhydration. Additionally, H 2 S influences key pathological processes such as inflammation, oxidative stress, and cell apoptosis. Dysregulation of endogenous H 2 S metabolism has been closely linked to the development of various vascular diseases, including aortic aneurysms, aortic dissection, atherosclerosis, and thrombotic conditions. Various endogenous and exogenous H 2 S donors have been developed, and these donors have demonstrated promising effects in preclinical models of vascular diseases such as atherosclerosis, pulmonary hypertension, and thrombosis by modulating oxidative stress, inflammatory pathways, and vascular remodeling. This review consolidates the current knowledge on the effects of H 2 S on vascular function and offers a comprehensive summary of recent advancements in the development and application of H 2 S donors in vascular disease research.","PeriodicalId":15212,"journal":{"name":"Journal of Cardiovascular Pharmacology","volume":" ","pages":""},"PeriodicalIF":2.2,"publicationDate":"2025-05-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12333525/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101825","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0