Cardiovascular Drugs and Therapy最新文献

{"title":"Finerenone After FINE-ONE and CONFIDENCE: Updating the Cardiorenal-Metabolic Treatment Paradigm Beyond Type 2 Diabetes.","authors":"Siddarth Raajasekar","doi":"10.1007/s10557-026-07924-0","DOIUrl":"10.1007/s10557-026-07924-0","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"2109-2110"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148618593","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":"Methodological Considerations Regarding Electrophysiological Assessment and Outcome Interpretation in AF-HFpEF Treated with Dapagliflozin Plus Sacubitril/Valsartan.","authors":"Tong Su, Tiantian Jia, Danping Xu","doi":"10.1007/s10557-026-07926-y","DOIUrl":"10.1007/s10557-026-07926-y","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"2111-2112"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148653212","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":"Monocyte Activation Drives Atrial Fibrillation in Hypertension.","authors":"Qian-Wan Deng, Zi-Qi Xu, Wei Zhang, Yuan-Yuan Kang, Wu-Wei Rong, Jia-Hui Xia, Ping-Jin Gao, Xiao-Dong Li, Ji-Guang Wang","doi":"10.1007/s10557-026-07867-6","DOIUrl":"10.1007/s10557-026-07867-6","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"1793-1808"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147493783","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":"Letter to \"NR1D2 Knockdown Alleviates Myocardial Infarction Through Nrf2 Signaling Pathway Activation\".","authors":"Minxia Zhao","doi":"10.1007/s10557-026-07931-1","DOIUrl":"10.1007/s10557-026-07931-1","url":null,"abstract":"<p><p>Targeting iron-dependent ferroptosis represents a promising strategy to limit myocardial infarction (MI) injury. Wang et al. recently demonstrated that silencing the circadian receptor NR1D2 (REV-ERBβ) preserves ischemic myocardium by activating the Nrf2/GPX4 antioxidant axis. While their mechanistic rigor is commendable, translating NR1D2 modulation to the clinic reveals a pharmacological paradox. Prior studies show that NR1D2 agonists also prevent post-MI heart failure via metabolic remodeling, contrasting with the benefits of NR1D2 inhibition reported here. We argue this discrepancy hinges on temporal specificity: acute knockdown likely halts immediate ferroptotic damage and subsequent DAMP-driven sterile inflammation, whereas subacute agonism supports metabolic recovery. Moving beyond the bench, systemic Nrf2 hyperactivation poses oncogenic risks, and compensatory NR1D1 upregulation may undermine long-term efficacy. Consequently, realizing the therapeutic potential of the NR1D2/Nrf2 axis requires mapping its dynamic post-MI expression to define exact intervention windows, alongside engineering cardiac-homing nanocarriers to bypass systemic toxicity and ensure precise myocardial salvage.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"2113-2114"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148705557","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":"Finerenone in Cardiorenal Disease: A Narrative Review of Molecular Mechanisms, Clinical Evidence, and Emerging Therapeutic Roles.","authors":"Giulio Geraci, Nicola Sinatra, Valentina Paternò, Vincenzo Calabrese, Giuliano Cassataro, Giuseppe Cuttone, Calogero Geraci, Roberta Esposito, Costantino Mancusi, Giacomo Pucci, Luca Zanoli, Giuseppe Mulè, Riccardo Polosa, Pietro Ferrara, Caterina Carollo","doi":"10.1007/s10557-026-07890-7","DOIUrl":"10.1007/s10557-026-07890-7","url":null,"abstract":"<p><p>Cardiorenal disease reflects a tightly interconnected pathophysiological continuum driven by neurohormonal activation, inflammation, oxidative stress, and progressive fibrosis. Among these mechanisms, mineralocorticoid receptor (MR) overactivation has emerged as a central mediator of cardiac and renal injury independent of blood pressure effects. Finerenone, a non-steroidal selective MR antagonist, exhibits distinct pharmacological properties compared with steroidal MR antagonists, including enhanced receptor selectivity, balanced cardiac and renal tissue distribution, and differential cofactor modulation that translates into potent anti-inflammatory and antifibrotic activity with an improved safety profile.Large outcome trials have established finerenone as an effective cardiorenal protective therapy. The FIDELIO-DKD and FIGARO-DKD trials demonstrated significant reductions in kidney disease progression and cardiovascular events in patients with type 2 diabetes and chronic kidney disease, with consistent benefits confirmed in the pooled FIDELITY analysis. More recently, the FINEARTS-HF trial extended these benefits to patients with heart failure with mildly reduced or preserved ejection fraction regardless of diabetes status. Across trials, hyperkalemia was infrequent when structured monitoring strategies were applied.Beyond established indications, emerging data suggest potential systemic effects on retinal and hepatic outcomes, while ongoing studies are evaluating finerenone in non-diabetic chronic kidney disease. Subgroup analyses consistently demonstrate preserved efficacy and favorable safety when finerenone is combined with sodium-glucose cotransporter-2 inhibitors, supporting complementary disease-modifying strategies.This review integrates molecular mechanisms, clinical trial evidence, systemic effects, and therapeutic positioning of finerenone within contemporary cardiorenal care, highlighting its expanding role in multidrug approaches targeting the cardiovascular-renal-metabolic axis.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"2061-2076"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13578082/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147986745","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":"Interpreting Mitochondrial Bioenergetics in Ischaemia-Reperfusion Injury: Caution on Causality and Methodological Consistency.","authors":"Malaha Ali","doi":"10.1007/s10557-026-07891-6","DOIUrl":"10.1007/s10557-026-07891-6","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"2097-2098"},"PeriodicalIF":3.5,"publicationDate":"2026-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147986704","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":"PDK4-Associated Metabolic Reprogramming Contributes to Lactate Accumulation and Parthanatos-Related Changes in Septic Cardiomyocytes.","authors":"Shaodong Yang, Cairong Yan, Zhenwei Xu, Tianbao Huang, Jintu Chen, Jingfa Zhu","doi":"10.1007/s10557-026-07970-8","DOIUrl":"https://doi.org/10.1007/s10557-026-07970-8","url":null,"abstract":"<p><strong>Background: </strong>Sepsis-related myocardial injury (SRMI) is characterized by metabolic reprogramming and cardiomyocyte death, but the relationship between these processes remains unclear. This study investigated the association between pyruvate dehydrogenase kinase 4 (PDK4)-related metabolic dysregulation and parthanatos-related changes in SRMI.</p><p><strong>Methods: </strong>SRMI was modeled using cecal ligation and perforation in mice and lipopolysaccharide-stimulated H9c2 cells. Myocardial injury, metabolic alterations, mitochondrial dysfunction, and parthanatos-related changes were assessed using RNA sequencing, histopathology, transmission electron microscopy, biochemical assays, Western blotting, RT-qPCR, immunofluorescence, and flow cytometry. PDK4 was silenced using siRNA in LPS-stimulated H9c2 cells for functional validation.</p><p><strong>Results: </strong>PDK4 was significantly upregulated in septic myocardium. This change was accompanied by increased PDH phosphorylation, pyruvate and lactate accumulation, ATP depletion, and mitochondrial ultrastructural damage. PAR accumulation increased, NAD⁺ levels decreased, and AIF/MIF nuclear translocation was enhanced, indicating prominent parthanatos-related changes. In LPS-stimulated H9c2 cells, PDK4 knockdown decreased the p-PDH/PDH ratio and lactate levels while increasing ATP levels. PDK4 silencing also reduced PAR accumulation, increased NAD⁺ levels, and decreased AIF/MIF nuclear translocation.</p><p><strong>Conclusion: </strong>PDK4 contributes to metabolic dysregulation and parthanatos-related changes in septic cardiomyocytes. However, whether lactate directly mediates the relationship between PDK4 and parthanatos requires further rescue experiments.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149079759","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":"Herpes Zoster Vaccination as Cardiovascular Prevention in Adults with Heart Disease.","authors":"Lorenzo Facila Rubio, Vicente Pallarés-Carratalá, Alberto Cordero, José Pérez Silvestre, Clara Bonanad Lozano","doi":"10.1007/s10557-026-07966-4","DOIUrl":"https://doi.org/10.1007/s10557-026-07966-4","url":null,"abstract":"<p><strong>Purpose: </strong>To summarize the evidence linking herpes zoster (HZ) with cardiovascular events and assess whether HZ vaccination may reduce cardiovascular risk, with particular attention to the transition from live attenuated vaccine (ZVL) to adjuvanted recombinant vaccine (RZV).</p><p><strong>Methods: </strong>Narrative review structured around SANRA quality domains, based on searches of PubMed/MEDLINE, Embase, Cochrane CENTRAL, ClinicalTrials.gov, and guideline and grey-literature sources through 12 August 2026, with two peer-review-identified sources added thereafter.</p><p><strong>Results: </strong>HZ is associated with a transient increase in stroke and myocardial infarction risk, particularly after ophthalmic HZ. The strongest population-level cardiovascular evidence concerns ZVL, with a South Korean cohort showing reductions in major cardiovascular events, heart failure, and stroke sustained for up to 8 years; ZVL is now withdrawn in the United States and European Union. A natural-experiment study directly comparing the platforms found a further 9% reduction in cardiovascular burden with RZV versus ZVL over 7 years. Real-world cohorts in high-risk populations and a peer-reviewed meta-analysis also support cardiovascular benefit, although most pooled analyses combine RZV and ZVL, and no randomized trial has been designed specifically for cardiovascular outcomes.</p><p><strong>Conclusion: </strong>Evidence increasingly supports a cardiovascular benefit of HZ vaccination, including with RZV currently in use, but remains predominantly observational or quasi-experimental. Dedicated randomized cardiovascular-outcome trials are needed.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149073734","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":"Reply to Letter to the Editor: In-Hospital SGLT-2 Inhibitor Initiation in Acute Heart Failure.","authors":"Muhammad Owais, Maham Altaf, Hafiz M Ahmed","doi":"10.1007/s10557-026-07964-6","DOIUrl":"https://doi.org/10.1007/s10557-026-07964-6","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058470","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":"Beyond KPAQ Improvement: Reassessing the Clinical Meaning of Cilostazol-Rosuvastatin Combination Therapy in Symptomatic Peripheral Artery Disease.","authors":"Junao Chen","doi":"10.1007/s10557-026-07965-5","DOIUrl":"https://doi.org/10.1007/s10557-026-07965-5","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":""},"PeriodicalIF":3.5,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149058556","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}