Cardiovascular Drugs and Therapy最新文献

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From Mechanism to Therapy: Establishing an Integrated Framework for the Regulation and Intervention of Matrix Vesicles in Vascular Calcification. 从机制到治疗:建立基质囊泡在血管钙化中的调控和干预的综合框架。
IF 3.5 3区 医学
Cardiovascular Drugs and Therapy Pub Date : 2026-10-01 Epub Date: 2026-04-27 DOI: 10.1007/s10557-026-07881-8
Mincheng Yu, Jingzheng Chen, Xinyue Wang, Ling Chen, Xiaomei Ren, Mayibai Mushajiang, Liqun Ren, Zhongqun Wang
{"title":"From Mechanism to Therapy: Establishing an Integrated Framework for the Regulation and Intervention of Matrix Vesicles in Vascular Calcification.","authors":"Mincheng Yu, Jingzheng Chen, Xinyue Wang, Ling Chen, Xiaomei Ren, Mayibai Mushajiang, Liqun Ren, Zhongqun Wang","doi":"10.1007/s10557-026-07881-8","DOIUrl":"10.1007/s10557-026-07881-8","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"2009-2028"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763323","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Possible clinical drug interactions between ticagrelor and concomitant medications: for adverse drug event monitoring in real-world. 替格瑞洛与伴随药物之间可能的临床药物相互作用:用于现实世界药物不良事件监测。
IF 3.5 3区 医学
Cardiovascular Drugs and Therapy Pub Date : 2026-10-01 Epub Date: 2026-04-21 DOI: 10.1007/s10557-026-07871-w
Tianya Liu, Zhuang Chen, Rui Wang, Xiaomei Xu, Fang Gao, Jie Zu, Zhiping Wang, Yiming Tian
{"title":"Possible clinical drug interactions between ticagrelor and concomitant medications: for adverse drug event monitoring in real-world.","authors":"Tianya Liu, Zhuang Chen, Rui Wang, Xiaomei Xu, Fang Gao, Jie Zu, Zhiping Wang, Yiming Tian","doi":"10.1007/s10557-026-07871-w","DOIUrl":"10.1007/s10557-026-07871-w","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1809-1823"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147763329","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
E3 Ubiquitin Ligase UBR5 Aggravates Cardiac Hypertrophy Via Inhibiting Nrf2/HO-1 Pathway. E3泛素连接酶UBR5通过抑制Nrf2/HO-1通路加重心肌肥厚。
IF 3.5 3区 医学
Cardiovascular Drugs and Therapy Pub Date : 2026-10-01 Epub Date: 2026-03-13 DOI: 10.1007/s10557-026-07852-z
Guofeng Zhu, Haiyang Fang, Congcong Xu, Kai Zhu, Tieqiu Huang, Wei Zhou, Min Huang
{"title":"E3 Ubiquitin Ligase UBR5 Aggravates Cardiac Hypertrophy Via Inhibiting Nrf2/HO-1 Pathway.","authors":"Guofeng Zhu, Haiyang Fang, Congcong Xu, Kai Zhu, Tieqiu Huang, Wei Zhou, Min Huang","doi":"10.1007/s10557-026-07852-z","DOIUrl":"10.1007/s10557-026-07852-z","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1669-1683"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147455312","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Cardioprotection Through Mitochondrial Modulation: A Systematic Review of Pharmacological Interventions in Animal Models of I/R Injury. 通过线粒体调节的心脏保护:I/R损伤动物模型的药物干预的系统综述。
IF 3.5 3区 医学
Cardiovascular Drugs and Therapy Pub Date : 2026-10-01 Epub Date: 2026-03-04 DOI: 10.1007/s10557-026-07851-0
Trissha Ybanez, Joshua Ingles, Eugene Du Toit, Jason Peart
{"title":"Cardioprotection Through Mitochondrial Modulation: A Systematic Review of Pharmacological Interventions in Animal Models of I/R Injury.","authors":"Trissha Ybanez, Joshua Ingles, Eugene Du Toit, Jason Peart","doi":"10.1007/s10557-026-07851-0","DOIUrl":"10.1007/s10557-026-07851-0","url":null,"abstract":"<p><strong>Purpose: </strong>Myocardial reperfusion following ischaemia paradoxically exacerbates mitochondrial and thus cardiac dysfunction. Although various treatment strategies have been utilised to prevent irreversible myocardial injury, translation to positive clinical trial outcomes has been unsuccessful. This systematic review aimed to evaluate pharmacological interventions in animal models of ischaemia-reperfusion (I/R), with emphasis on cardiac and cell death outcomes and direct assessment of mitochondrial bioenergetics.</p><p><strong>Methods: </strong>Search terms were entered into PubMed, Scopus, Embase and Web of Science. Screening, data extraction and quality assessment of papers were conducted according to the inclusion and exclusion criteria selected for this study. Eighteen papers from a total of 1571 studies were included. These studies investigated 15 drugs of interest in animals subjected to either in vivo or ex vivo I/R. Mitochondrial function parameters were assessed by measuring either mitochondrial respiration and/or enzyme activity, with 4 of these also assessing electron transport chain protein expression.</p><p><strong>Results: </strong>Pharmaceuticals preserved mitochondrial respiratory capacity by directly targeting the electron transport chain complexes or indirectly via proteins involved in canonical cardioprotective pathways. This led to improved post-ischaemic cardiac function and reductions in markers of cellular injury and myocardial infarction.</p><p><strong>Conclusion: </strong>Multi-targeted manipulation of components of mitochondrial signalling and function evidently reduces I/R injury. Quality assessment of most papers revealed an unclear risk of bias due to inadequate reporting of study parameters. Clear and consistent reporting of study outcomes, specifically mitochondrial bioenergetics across all experimental stages, is essential to enhance the translational potential of mitoprotective compounds in the clinical treatment of I/R.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1861-1880"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13578120/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147354060","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Unmeasured Confounders and Control Group Heterogeneity in Laser-Assisted Lead Extraction. 激光辅助铅提取中未测量的混杂因素和对照组异质性。
IF 3.5 3区 医学
Cardiovascular Drugs and Therapy Pub Date : 2026-10-01 Epub Date: 2026-04-16 DOI: 10.1007/s10557-026-07873-8
Yinglei Lin
{"title":"Unmeasured Confounders and Control Group Heterogeneity in Laser-Assisted Lead Extraction.","authors":"Yinglei Lin","doi":"10.1007/s10557-026-07873-8","DOIUrl":"10.1007/s10557-026-07873-8","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"2089-2090"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147697878","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Screening of Anti-atherosclerosis Drugs Based on the Apolipoprotein apoeb Gene Knockout Zebrafish Model. 基于载脂蛋白apoeb基因敲除斑马鱼模型的抗动脉粥样硬化药物筛选。
IF 3.5 3区 医学
Cardiovascular Drugs and Therapy Pub Date : 2026-10-01 Epub Date: 2026-03-10 DOI: 10.1007/s10557-026-07847-w
Haoyan Wang, Jiufeng Yin, Hui Wang, Mingkai Li, Xinyi Zhang, Feng Zhao, Wenqing Yang
{"title":"Screening of Anti-atherosclerosis Drugs Based on the Apolipoprotein apoeb Gene Knockout Zebrafish Model.","authors":"Haoyan Wang, Jiufeng Yin, Hui Wang, Mingkai Li, Xinyi Zhang, Feng Zhao, Wenqing Yang","doi":"10.1007/s10557-026-07847-w","DOIUrl":"10.1007/s10557-026-07847-w","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1651-1668"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147430775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Uncertainty Regarding the Safety of SGLT-2 Inhibitors Prior to PCI: the Impact of Unmeasured Confounding and Statistical Power. PCI术前SGLT-2抑制剂安全性的不确定性:未测量混杂因素和统计威力的影响
IF 3.5 3区 医学
Cardiovascular Drugs and Therapy Pub Date : 2026-10-01 Epub Date: 2026-01-30 DOI: 10.1007/s10557-026-07846-x
Jun Tang
{"title":"Uncertainty Regarding the Safety of SGLT-2 Inhibitors Prior to PCI: the Impact of Unmeasured Confounding and Statistical Power.","authors":"Jun Tang","doi":"10.1007/s10557-026-07846-x","DOIUrl":"10.1007/s10557-026-07846-x","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"2081-2082"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146084435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
Hyperuricemia and Hypoxic Pulmonary Hypertension: Pathogenic Links, Clinical Evidence, and Emerging Therapeutic Insights. 高尿酸血症和低氧性肺动脉高压:致病联系、临床证据和新出现的治疗见解。
IF 3.5 3区 医学
Cardiovascular Drugs and Therapy Pub Date : 2026-10-01 Epub Date: 2026-03-06 DOI: 10.1007/s10557-026-07859-6
Zhanpeng Cao, Wei Ma, Chuanchuan Liu
{"title":"Hyperuricemia and Hypoxic Pulmonary Hypertension: Pathogenic Links, Clinical Evidence, and Emerging Therapeutic Insights.","authors":"Zhanpeng Cao, Wei Ma, Chuanchuan Liu","doi":"10.1007/s10557-026-07859-6","DOIUrl":"10.1007/s10557-026-07859-6","url":null,"abstract":"<p><strong>Purpose: </strong>This review aims to explore the role of hyperuricemia in the pathogenesis of hypoxic pulmonary hypertension (HPH), focusing on its contribution to pulmonary vascular remodeling and evaluating the potential of uric acid-lowering strategies.</p><p><strong>Methods: </strong>A comprehensive review of the literature was conducted to assess the impact of elevated uric acid levels on HPH. The review highlights uric acid's effects on smooth muscle cell proliferation, endothelial dysfunction, oxidative stress, and inflammation. It also examines the interference of uric acid with nitric oxide signaling and its activation of the renin-angiotensin system under hypoxic conditions.</p><p><strong>Results: </strong>The literature indicates a significant correlation between elevated serum uric acid levels and the severity of HPH. Uric acid contributes to vascular remodeling by promoting oxidative stress, inflammation, and endothelial dysfunction. Preclinical evidence suggests that uric acid-lowering interventions, when combined with antioxidant or anti-inflammatory therapies, may reduce pulmonary vascular damage and improve outcomes.</p><p><strong>Conclusion: </strong>Uric acid represents a potential therapeutic target for HPH. Uric acid-lowering strategies, although promising, require further clinical validation. A deeper understanding of the molecular mechanisms underlying hyperuricemia in HPH may facilitate the development of targeted diagnostic and therapeutic approaches.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1881-1897"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147363923","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
The Nonlinear Relationship Between Serum Uric Acid and Cardiovascular Disease Risk: Mechanistic Insights and Clinical Implications. 血清尿酸与心血管疾病风险的非线性关系:机制见解和临床意义。
IF 3.5 3区 医学
Cardiovascular Drugs and Therapy Pub Date : 2026-10-01 Epub Date: 2026-03-16 DOI: 10.1007/s10557-026-07866-7
Chunyan Hou, Zhiwei Zheng, Xiaoqian Zheng, Menghua Liu, Shuling Xu, Rumeng Chen, Meihua Bao, Chunxia Huang, Sen Li
{"title":"The Nonlinear Relationship Between Serum Uric Acid and Cardiovascular Disease Risk: Mechanistic Insights and Clinical Implications.","authors":"Chunyan Hou, Zhiwei Zheng, Xiaoqian Zheng, Menghua Liu, Shuling Xu, Rumeng Chen, Meihua Bao, Chunxia Huang, Sen Li","doi":"10.1007/s10557-026-07866-7","DOIUrl":"10.1007/s10557-026-07866-7","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1917-1926"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147466851","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
NR1D2 Knockdown Alleviates Myocardial Infarction through Nrf2 Signaling Pathway Activation. NR1D2敲低通过激活Nrf2信号通路缓解心肌梗死。
IF 3.5 3区 医学
Cardiovascular Drugs and Therapy Pub Date : 2026-10-01 Epub Date: 2026-05-04 DOI: 10.1007/s10557-026-07879-2
Ting Wang, Helong Xiao, Meijian Yang, Jing Liu, Yang Yang
{"title":"NR1D2 Knockdown Alleviates Myocardial Infarction through Nrf2 Signaling Pathway Activation.","authors":"Ting Wang, Helong Xiao, Meijian Yang, Jing Liu, Yang Yang","doi":"10.1007/s10557-026-07879-2","DOIUrl":"10.1007/s10557-026-07879-2","url":null,"abstract":"<p><strong>Purpose: </strong>Ferroptosis contributes to myocardial infarction (MI) pathogenesis. However, the role of nuclear receptor subfamily 1 group D member 2 (NR1D2) in MI-associated ferroptosis and its potential interaction with nuclear factor erythroid 2-related factor 2 (Nrf2) pathway remains unclear. We sought to determine whether NR1D2 regulates ferroptosis in MI through the Nrf2 pathway and to evaluate the therapeutic potential of NR1D2 knockdown.</p><p><strong>Methods: </strong>Bioinformatic analyses of GEO datasets identified NR1D2 as a key ferroptosis-related gene in MI. In vitro, NR1D2 expression was silenced in HL-1 cardiomyocytes subjected to hypoxia/reoxygenation (H/R) injury. Nrf2 inhibitor ML385 was used to verify pathway involvement. A mouse model of MI was established, and cardiac function was assessed following NR1D2 knockdown with or without ML385 co-treatment.</p><p><strong>Results: </strong>NR1D2 expression was significantly upregulated in MI. Its knockdown in H/R-injured cardiomyocytes reduced cell death, inflammation, and ferroptosis, as indicated by decreased Fe²⁺ and malondialdehyde levels and elevated GSH/GSSG ratio. These protective effects were abolished by ML385, confirming Nrf2 dependence. Mechanistically, NR1D2 knockdown activated the Nrf2/HO-1 signaling axis, leading to the upregulation of downstream effectors glutathione peroxidase 4and SLC7A11. In MI mice, NR1D2 knockdown improved cardiac function (increased EF and FS), decreased infarct size, and inhibited ferroptosis-effects that were also negated by ML385.</p><p><strong>Conclusion: </strong>NR1D2 aggravates MI injury by suppressing the Nrf2 pathway and promoting ferroptosis. Targeting NR1D2 activates Nrf2 signaling and alleviates ferroptotic damage, revealing a novel regulatory mechanism and identifying NR1D2 as a promising therapeutic target for MI.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1729-1746"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147811493","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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
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