Cardiovascular Drugs and Therapy最新文献

{"title":"Antithrombotic therapy after valve-in-valve TAVI: discharge regimen as a marker of phenotype.","authors":"Artur Dziewierz, Kamil Skowron, Tomasz Rakowski","doi":"10.1007/s10557-026-07936-w","DOIUrl":"https://doi.org/10.1007/s10557-026-07936-w","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148757981","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":"Competing Risks, Renal Function, and Register Completeness: Methodological Considerations for Drug-Drug Interactions in Older Adults with Atrial Fibrillation.","authors":"Muhammad Adil Choudhry","doi":"10.1007/s10557-026-07930-2","DOIUrl":"https://doi.org/10.1007/s10557-026-07930-2","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705502","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":"Unveiling the miR‑26a‑5p/MSMO1/7‑DHC Axis: A Novel Therapeutic Target in Myocardial Ischemia-Reperfusion Injury.","authors":"Yonglin Fu, Bingjie Han, Jiankai Zhang, Lu Liu, Wenjie Chen, Ciying Kuang, Mei Jiang, Xiaojun Cui","doi":"10.1007/s10557-026-07922-2","DOIUrl":"https://doi.org/10.1007/s10557-026-07922-2","url":null,"abstract":"<p><p>Ferroptosis plays a critical role in myocardial ischemia-reperfusion injury (MIRI). Here, we discovered that MSMO1, a key enzyme in the cholesterol biosynthesis pathway, regulates ferroptosis in MIRI, and identified miR-26a-5p as an upstream regulator of MSMO1. During MIRI, downregulation of miR-26a-5p led to suppression of MSMO1, reduction of 7-DHC accumulation, and promotion of lipid peroxidation and ferroptosis. To translate this mechanism, we developed engineered exosomes delivering miR-26a-5p. In cellular and mouse MIRI models, this intervention significantly attenuated serum levels of cardiac injury biomarkers (cTnI and CK-MB), restored systemic antioxidant capacity, and attenuated early myocardial fibrosis. This work provides a novel therapeutic strategy for MIRI and provides preclinical evidence supporting the potential of engineered exosomes as a cell-free therapeutic platform.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148700770","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":"Stroke Heart Syndrome: Neuroimmune and Metabolic Crosstalk with Conceptual Approaches for Precision Therapeutics.","authors":"Qiwen Nie, Wang Guo, Zhihao Wang, Hongxin Li, Hongyu Li","doi":"10.1007/s10557-026-07929-9","DOIUrl":"https://doi.org/10.1007/s10557-026-07929-9","url":null,"abstract":"<p><strong>Background: </strong>Stroke-heart syndrome (SHS) represents a serious complication after stroke that significantly elevates mortality risk, especially in the short term. The primary initiating pathological event in SHS is acute ischemic stroke, which subsequently triggers secondary cardiac dysfunction through a complex and continuous interplay among the brain, the immune system, and systemic metabolism.</p><p><strong>Pathophysiological mechanisms: </strong>In the acute phase, an acute surge of stress hormones such as norepinephrine induces calcium overload and subsequent myocardial damage. Meanwhile, a progressive cardiac remodeling process begins, which continues to evolve over subsequent weeks. Subacutely, systemic immune activation drives splenic leukocyte mobilization and the formation of neutrophil extracellular traps (NETs), thereby exacerbating inflammation and plaque instability. Over time, gut microbiota derived metabolites, particularly phenylacetylglutamine (PAGln), may further aggravate thrombotic risk and cardiac metabolic vulnerability.</p><p><strong>Endophenotype-based framework and interventions: </strong>To address this multifactorial complexity, this review proposes a hypothesis-generating conceptual framework that categorizes SHS into three endophenotypes, including neurogenic arrhythmic (Type I), inflammatory thrombotic (Type II), and metabolic remodeling (Type III). Potential phenotype-specific interventions include beta blockers for neural stabilization, NETs degradation for immunomodulation, and metabolic pathway antagonists.</p><p><strong>Challenges and perspectives: </strong>Although interventions like remote ischemic conditioning (RIC) demonstrate promising biological activity and safety in preclinical evaluations, translating these exploratory findings into consistent clinical outcomes remains a significant translational challenge. Furthermore, sex specific mechanisms, notably the altered estrogen signaling in women, highlight the potential need for tailored therapeutic strategies. Transitioning toward this etiology-based paradigm provides an essential foundation for future precision therapeutics, aiming to mitigate targeted pathophysiological drivers rather than relying solely on generalized cardioprotection.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148676821","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":"Lentinan Attenuates Experimental Atherosclerosis by Regulating Macrophage HCK/GUSB Expression and Amino Acid Metabolic Remodeling.","authors":"Guoling Rong, Jiaolong Yu, Cai Jing, Lili Liu, Bingguang Zhong, Runwen Li","doi":"10.1007/s10557-026-07925-z","DOIUrl":"https://doi.org/10.1007/s10557-026-07925-z","url":null,"abstract":"<p><p>Atherosclerosis (AS) is a chronic inflammatory vascular disease characterized by lipid accumulation, immune activation, and plaque formation. This study investigated the anti-atherosclerotic effects of Lentinan (LNT) and explored its potential macrophage-associated mechanisms. In high-fat diet-fed ApoE⁻/⁻ mice, LNT markedly attenuated aortic plaque formation, lipid deposition, serum pro-inflammatory cytokine levels, and dyslipidemia, indicating a protective effect against AS progression. Integrated target screening and transcriptomic analyses identified HCK and GUSB as key candidate targets associated with the response to LNT. Both genes were upregulated in atherosclerotic tissues and were further assessed in an independent human dataset. Experimental validation in ApoE⁻/⁻ mouse aortic tissues showed that LNT reduced HCK and GUSB expression, while single-cell transcriptomic analysis indicated that both genes were predominantly enriched in macrophage populations within atherosclerotic lesions. In ox-LDL-induced RAW264.7 foam cells, LNT decreased intracellular lipid accumulation and downregulated HCK and GUSB expression, further supporting a macrophage-related protective mechanism. In addition, targeted metabolomic analysis suggested that LNT reshaped amino acid metabolism, which may contribute to improvement of the inflammatory and immunometabolic microenvironment in AS. Molecular docking and molecular dynamics simulations further indicated potential interactions between LNT and HCK/GUSB. Overall, these findings suggest that LNT attenuates experimental atherosclerosis by regulating macrophage-associated HCK/GUSB expression, suppressing foam cell formation, and modulating amino acid metabolic remodeling.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148676848","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":"Endpoint Inconsistency and Overinterpretation of Early Biomarkers After CABG.","authors":"Yuxin Sheng, Le Wen","doi":"10.1007/s10557-026-07921-3","DOIUrl":"https://doi.org/10.1007/s10557-026-07921-3","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148668544","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":"PRMT2 Aggravates Pressure Overload-induced Cardiac Remodeling by Promoting Endothelial Phenotypic Transition via Snail1 Methylation.","authors":"Xianwei Fan, Xuejie Li, Juan Hu, Lijie Yan, Jintao Wu, Leiming Zhang, Jingjing Liu, Haitao Yang","doi":"10.1007/s10557-026-07928-w","DOIUrl":"https://doi.org/10.1007/s10557-026-07928-w","url":null,"abstract":"<p><strong>Purpose: </strong>Endothelial-to-mesenchymal transition (EndMT) is implicated in cardiac remodeling under pathological stress, although its full in vivo occurrence may be context-dependent. Emerging evidence suggests that protein methylation is an important post-translational modification involved in regulating endothelial phenotypic transition (EndMT-like process). However, the role of protein arginine methyltransferase 2 (PRMT2), a key protein arginine methyltransferase, in modulating endothelial phenotypic transition-particularly in the context of cardiac remodeling-remains poorly understood.</p><p><strong>Methods: </strong>A transverse aortic constriction (TAC) mouse model was used to induce cardiac remodeling, and adeno-associated virus serotype 9 (AAV9) was administered to specifically silence PRMT2 in endothelial cells.</p><p><strong>Results: </strong>We found that PRMT2 expression was significantly upregulated in cardiac endothelial cells following pressure overload. Endothelial-specific silencing of PRMT2 markedly attenuated cardiac hypertrophy, fibrosis, and endothelial phenotypic transition in TAC mice. In vitro, PRMT2 knockdown in isolated murine cardiac microvascular endothelial cells alleviated TGF-β1-induced endothelial phenotypic transition, while PRMT2 overexpression exacerbated these phenotypic changes. Mechanistically, PRMT2 enhanced endothelial phenotypic transition by promoting monomethylation of Snail1 and activation of the Snail signaling pathway. Importantly, endothelial-specific knockdown of Snail1 reversed the phenotypic transition induced by PRMT2 overexpression.</p><p><strong>Conclusion: </strong>These findings identify PRMT2 as a key epigenetic regulator of endothelial phenotypic transition in cardiac remodeling, suggesting it may serve as a potential therapeutic target for heart failure.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-08-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148663443","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":"Tenecteplase Before Endovascular Thrombectomy (EVT): A Step Forward in Acute Stroke Management.","authors":"Muhammad Zubair","doi":"10.1007/s10557-025-07748-4","DOIUrl":"10.1007/s10557-025-07748-4","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1211"},"PeriodicalIF":3.5,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144607449","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":"Further Considerations on Cardioprotective Effect of Aloperine Against Myocardial Ischemia/Reperfusion Injury.","authors":"Yu Hu, Tai Li, Chao Wu","doi":"10.1007/s10557-025-07752-8","DOIUrl":"10.1007/s10557-025-07752-8","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1215-1216"},"PeriodicalIF":3.5,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667258","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":"The 2025 ESC/EAS Dyslipidaemia Focused Update: Clinical Interpretation and Practical Implications.","authors":"Luca Bonanni, Ada Cutolo, Nicola Ferri","doi":"10.1007/s10557-026-07855-w","DOIUrl":"10.1007/s10557-026-07855-w","url":null,"abstract":"<p><p>The 2025 ESC/EAS Dyslipidaemia Focused Update provides a targeted revision of the 2019 guidelines, integrating newly available evidence with the potential to influence clinical decision-making before the next full update. While LDL-C treatment targets remain unchanged, the document reshapes how they should be achieved, emphasizing faster therapeutic intensification, broader use of combination therapy and improved risk stratification with SCORE2/SCORE2-OP, lipoprotein(a) [Lp(a)] and coronary artery calcium (CAC) scoring. New evidence supporting bempedoic acid, inclisiran and evinacumab expands the therapeutic armamentarium, particularly for patients at high, very high and extreme cardiovascular risk or those with statin intolerance. In the acute coronary syndrome (ACS) setting, the update reinforces a more proactive, early-intensification approach. Overall, the Focused Update refines the operational framework of LDL-C management, promoting earlier, more personalized and more sustained lipid lowering to reduce cumulative atherosclerotic exposure.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1629-1635"},"PeriodicalIF":3.5,"publicationDate":"2026-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146217971","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}