{"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}
{"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}
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}
{"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}
{"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}
{"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}
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}