Cardiovascular Drugs and Therapy最新文献

{"title":"Discharge of Acute Coronary Syndrome Patients on Sub-Optimal Dual Anti-Platelet Therapy: A Single Center Experience.","authors":"Jeffrey B Booker, Alexander J Nihart, Matthew J Campen, Eduardo Medrano-Rodriguez, James C Blankenship","doi":"10.1007/s10557-024-07563-3","DOIUrl":"10.1007/s10557-024-07563-3","url":null,"abstract":"<p><strong>Purpose: </strong>To identify and quantify the reasons why acute coronary syndrome (ACS) patients undergoing stenting at the University of New Mexico Hospital (UNMH) were prescribed sub-optimal dual antiplatelet therapy (DAPT) at discharge, and to identify practice patterns that could potentially lead to improved DAPT treatment for these patients.</p><p><strong>Methods: </strong>We reviewed electronic medical records and cardiac catheterization records of 326 patients who underwent percutaneous coronary intervention (PCI) at UNMH between January 1, 2021, and June 30, 2022 and identified 229 ACS patients who survived until discharge. Demographic and clinical characteristics relevant to P2Y₁₂ inhibitor selection were obtained from a review of medical records. Pharmacists' notes documenting their efforts to secure appropriate insurance coverage and reasons for discharging patients on clopidogrel rather than ticagrelor/prasugrel were reviewed. Patients discharged on aspirin and clopidogrel underwent review of medical records and cardiac catheterization lab records to determine if the discharge P2Y₁₂ drug was appropriate. Reasons for inappropriate discharge on clopidogrel were categorized as cost/insurance, patient preference, concern for daily adherence to a twice-daily medication, and maintenance of pre-hospital clopidogrel therapy rather than switch to ticagrelor after PCI.</p><p><strong>Results: </strong>The 229 ACS patients included 87 (38.0%) appropriately discharged on ticagrelor/prasugrel, 63 (27.5%) appropriately discharged on clopidogrel, 75 (32.8%) discharged on sub-optimal clopidogrel, and 4 (1.7%) not discharged on a P2Y₁₂ inhibitor. For patients inappropriately discharged on clopidogrel (n = 75), the most common reasons were cost or lack of insurance (n = 56) and clinical inertia (taking clopidogrel before PCI and maintained on it afterward) (n = 17). Sub-optimal P2Y₁₂ therapy at discharge was significantly associated with lack of insurance (odds ratio 21.5, 95% confidence interval 5.33-156,p < 0.001) but not with ethnicity, age, sex, or diabetes.</p><p><strong>Conclusion: </strong>At the University of New Mexico, a safety-net hospital, increasing financially restricted access to ticagrelor/prasugrel could help up to 24.5% of ACS patients reduce their risk of ischemic events. For patients admitted on clopidogrel DAPT, escalating to ticagrelor/prasugrel could reduce ischemic risk in 7.4%. Expanding and improving healthcare insurance coverage might reduce the frequency of discharge on sub-optimal P2Y₁₂ therapy.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"783-789"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140897431","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":"Are Sodium-Glucose Cotransporter-2 Inhibitors the Cherry on Top of Cardio-Oncology Care?","authors":"Carlos A Gongora, Lili Zhang, Juan Lopez Mattei, Enrique Ruiz-Mori, Gina Gonzalez-Robledo, Leandro Slipczuk, Joffre Lara, Jorge E Cossio-Aranda, Juan Badimon","doi":"10.1007/s10557-024-07604-x","DOIUrl":"10.1007/s10557-024-07604-x","url":null,"abstract":"<p><p>The increasing aging of the population combined with improvements in cancer detection and care has significantly improved the survival and quality of life of cancer patients. These benefits are hampered by the increase of cardiovascular diseases being heart failure the most frequent manifestation of cardiotoxicity and becoming the major cause of morbidity and mortality among cancer survivor. Current strategies to prevent cardiotoxicity involves different approaches such as optimal management of CV risk factors, use of statins and/or neurohormonal medications, and, in some cases, even the use of chelating agents. As a class, SGLT2-i have revolutionized the therapeutic horizon of HF patients independently of their ejection fraction or glycemic status. There is an abundance of data from translational and observational clinical studies supporting a potential beneficial role of SGLT2-i in mitigating the cardiotoxic effects of cancer patients receiving anthracyclines. These findings underscore the need for more robust clinical trials to investigate the effect on cardiovascular outcomes of the prophylactic SGLT2-i treatment in patients undergoing cancer treatment.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"849-856"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141490975","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":"MicroRNA-210-5p - a New Druggable Target for Pulmonary Hypertension?","authors":"Jose A Navarro-Garcia, Alexandra J Osborne, Xander H T Wehrens","doi":"10.1007/s10557-025-07701-5","DOIUrl":"10.1007/s10557-025-07701-5","url":null,"abstract":"","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"933-934"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143976849","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":"US Population Eligibility and Estimated Impact of Tirzepatide Treatment on Obesity Prevalence and Cardiovascular Disease Events.","authors":"Nathan D Wong, Hridhay Karthikeyan, Wenjun Fan","doi":"10.1007/s10557-024-07583-z","DOIUrl":"10.1007/s10557-024-07583-z","url":null,"abstract":"<p><strong>Purpose: </strong>Tirzepatide promotes weight loss and reduces risk factors for cardiovascular disease (CVD) in adults with overweight and obesity. We examined the number of US adults eligible for tirzepatide and its impact on obesity and CVD events.</p><p><strong>Methods: </strong>We identified US adults aged ≥ 18 years from the cross-sectional US National Health and Nutrition Examination Survey (NHANES) 2015-2018 eligible for tirzepatide based on SURMOUNT-1 trial eligibility criteria. Weight changes in SURMOUNT-1 from tirzepatide 15 mg treatment were used to project the impact on weight change and obesity prevalence in the population assuming titration to this dosage. We estimated 10-year CVD risks from BMI-based Framingham CVD risk scores before and after applying tirzepatide 15 mg treatment BMI and risk factor effects from SURMOUNT-1, the differences in estimated risks multiplied by the eligible NHANES weighted population representing the estimated \"preventable\" CVD events.</p><p><strong>Results: </strong>We identified 4015 US adults (estimated population size of 93.4 million [M]) to fit SURMOUNT-1 eligibility criteria, representing 38% of US adults. When the effects of 15 mg tirzepatide were applied, we estimated 70.6% (65.9 M) and 56.7% (53.0 M) of adults to show ≥ 15% and ≥ 20% reductions in weight, respectively, translating to 58.8% (55.0 M) fewer persons with obesity. Among those without CVD, estimated 10-year CVD risks were 10.1% \"before\" and 7.7% \"after\" tirzepatide \"treatment\" reflecting a 2.4% absolute (and 23.6% relative) risk reduction translating to 2.0 million preventable CVD events over 10 years.</p><p><strong>Conclusion: </strong>Tirzepatide treatment in appropriate US adults may substantially reduce obesity prevalence and CVD events, impacting beneficially on associated healthcare costs.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"837-847"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12296773/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141293131","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":"Quercetin Alleviates Cardiac Fibrosis via Regulating the SIRT3 Signaling Pathway.","authors":"Da-Wei Lin, Yi-Wen Jiang, Chen Wu, Hao Zhang, Ying-Ze Li, Yao-Sheng Wang","doi":"10.1007/s10557-024-07658-x","DOIUrl":"10.1007/s10557-024-07658-x","url":null,"abstract":"<p><strong>Purpose: </strong>Cardiovascular diseases, exacerbated by cardiac fibrosis, are the leading causes of mortality. We aimed to determine the role of quercetin (QU) in cardiac fibrosis and the underlying mechanism.</p><p><strong>Methods: </strong>In this study, 8-week-old mice were subjected to either transverse aortic constriction (TAC) or sham surgery, then they were administered QU or saline. Thereafter, cardiac function and cardiac hypertrophy were accessed. In vitro, cardiac fibroblasts (CFs) were treated with angiotensin II (Ang II) with or without QU. Western blot, qPCR, EdU incorporation assay, and immunofluorescence staining analysis were used to investigate the molecular and cellular features.</p><p><strong>Results: </strong>For the TAC mouse model, cardiac fibrosis was alleviated by QU. The study revealed that the trans-differentiation and proliferation of CFs promoted by Ang II would be reversed by QU in vitro. Mechanistically, QU exerted the anti-fibrotic effect by regulating the SIRT3/TGF-β/Smad3 signaling pathway.</p><p><strong>Conclusion: </strong>Quercetin protects against cardiac fibrosis by mediating the SIRT3 signaling pathway.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"737-748"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142827534","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":"Evinacumab Reduces Triglyceride-Rich Lipoproteins in Patients with Hyperlipidemia: A Post-Hoc Analysis of Three Randomized Clinical Trials.","authors":"Robert S Rosenson, Daniel J Rader, Shazia Ali, Poulabi Banerjee, Jennifer McGinniss, Robert Pordy","doi":"10.1007/s10557-024-07567-z","DOIUrl":"10.1007/s10557-024-07567-z","url":null,"abstract":"<p><strong>Purpose: </strong>Natural selection (Mendelian randomization) studies support a causal relationship between elevated triglyceride-rich lipoproteins (TRLs) and atherosclerotic cardiovascular disease (ASCVD). This post-hoc analysis assessed the efficacy of evinacumab in reducing TRLs in patient cohorts from three separate clinical trials with evinacumab.</p><p><strong>Methods: </strong>Patients with homozygous familial hypercholesterolemia (HoFH) and low-density lipoprotein cholesterol (LDL-C) ≥ 70 mg/dL were enrolled in a phase III trial (R1500-CL-1629; NCT03399786). Patients diagnosed with refractory hypercholesterolemia, with LDL-C ≥ 70 mg/dL or ≥ 100 mg/dL for those with or without ASCVD, respectively, were enrolled in a phase II trial (R1500-CL-1643; NCT03175367). Patients with severe hypertriglyceridemia (fasting TGs ≥ 500 mg/dL) were enrolled in a phase II trial (R1500-HTG-1522; NCT03452228). Patients received evinacumab intravenously (5 or 15 mg/kg) every 4 weeks, or subcutaneously (300 or 450 mg) every week or every 2 weeks. Efficacy outcomes included change in TRLs (calculated as total cholesterol minus high-density lipoprotein cholesterol minus LDL-C) and other lipid parameters from baseline to 12, 16, or 24 weeks for trial 1522, 1643, and 1629, respectively.</p><p><strong>Results: </strong>At baseline, TRL levels were higher for patients with severe hypertriglyceridemia entering the 1522 trial vs. other cohorts. Reductions in TRLs were observed across all studies with evinacumab, with > 50% reduction from baseline observed at the highest doses evaluated in patients with HoFH or refractory hypercholesterolemia. Within all three trials, evinacumab was generally well tolerated.</p><p><strong>Conclusions: </strong>Despite limitations in direct comparisons between study groups, these data indicate that TRL levels could be a future target for lipid-lowering therapies.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"925-931"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12297002/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140038782","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":"Enhanced Reendothelialization and Thrombosis Prevention with a New Drug-Eluting Stent.","authors":"Dunpeng Cai, Andy C Chen, Ruimei Zhou, Takashi Murashita, William P Fay, Shi-You Chen","doi":"10.1007/s10557-024-07584-y","DOIUrl":"10.1007/s10557-024-07584-y","url":null,"abstract":"<p><strong>Purpose: </strong>The objective of the study is to test the efficacy of cyclopentenyl cytosine (CPEC)-coated stents on blocking artery stenosis, promoting reendothelialization, and reducing thrombosis.</p><p><strong>Methods: </strong>Scanning electron microscopy was employed to observe the morphological characteristics of stents coated with a mixture of CPEC and poly(lactic-co-glycolic acid) (PLGA) copolymer. PLGA has been used in various Food and Drug Administration (FDA)-approved therapeutic devices. In vitro release of CPEC was tested to measure the dynamic drug elution. Comparison between CPEC- and everolimus-coated stents on neointimal formation and thrombosis formation was conducted after being implanted into the human internal mammary artery and grafted to the mouse aorta.</p><p><strong>Results: </strong>Optimization in stent coating resulted in uniform and consistent coating with minimal variation. In vitro drug release tests demonstrated a gradual and progressive discharge of CPEC. CPEC- or everolimus-coated stents caused much less stenosis than bare-metal stents. However, CPEC stent-implanted arteries exhibited enhanced reendothelialization compared to everolimus stents. Mechanistically, CPEC-coated stents reduced the proliferation of vascular smooth muscle cells while simultaneously promoting reendothelialization. More significantly, unlike everolimus-coated stents, CPEC-coated stents showed a significant reduction in thrombosis formation even in the absence of ongoing anticoagulant treatment.</p><p><strong>Conclusions: </strong>The study establishes CPEC-coated stent as a promising new device for cardiovascular interventions. By enhancing reendothelialization and preventing thrombosis, CPEC offers advantages over conventional approaches, including the elimination of the need for anti-clogging drugs, which pave the way for improved therapeutic outcomes and management of atherosclerosis-related medical procedures.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"765-774"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12381966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141236971","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":"Changes in Heart Rate Variability Parameters Following Radiofrequency Ablation in Patients with Atrial Fibrillation: A Systematic Review and Meta-Analysis.","authors":"Mahsa Mansourian, Zahra Teimouri-Jervekani, Azam Soleimani, Rasool Nouri, Hamidreza Marateb, Marjan Mansourian","doi":"10.1007/s10557-024-07549-1","DOIUrl":"10.1007/s10557-024-07549-1","url":null,"abstract":"<p><strong>Purpose: </strong>Radiofrequency (RF) ablation is a prevalent treatment for atrial fibrillation (AF), targeting triggers within the pulmonary vein (PV) for elimination. This study evaluated heart rate variability (HRV) parameter changes at three intervals post-RF ablation: short-term (immediately to 1 month), medium-term (1 to 6 months), and long-term (6 months to 1 year). We compared two ablation techniques: circumferential PV isolation (CPVI) and segmental PV isolation (SPVI).</p><p><strong>Methods: </strong>A thorough search of databases, including PubMed, Embase, Scopus, Web of Science, and Cochrane, in 2022 yielded 835 pertinent studies. After inclusion criteria were applied, 22 studies were analyzed.</p><p><strong>Results: </strong>Results showed a marked decline in HRV parameters post-AF ablation, with LF/HF as an exception. These reductions persisted in short- and long-term evaluations up to a year post-procedure. Subgroup analysis revealed significant HRV declines, with distinct LF/HF values post-SPVI.</p><p><strong>Conclusion: </strong>This meta-analysis suggests the potential of decreased HRV as an indicator of autonomic denervation, necessitating further exploration to optimize therapeutic strategies and enhance patient outcomes.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"887-901"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139575228","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":"Comparative Efficacy of Colchicine and Intensive Low-density Lipoprotein Cholesterol Lowering in Patients with Atherosclerotic Diseases receiving Statins: A Network Meta-analysis of Randomized Controlled Trials.","authors":"Zhenhong Ou, Fangchao Wang, Yunlin Chen, Xueyuan Liu, Boli Ran, Yuehui Yin, Kun Cui","doi":"10.1007/s10557-024-07622-9","DOIUrl":"10.1007/s10557-024-07622-9","url":null,"abstract":"<p><strong>Aims: </strong>Adding intensive low-density lipoprotein cholesterol (LDL-C)-lowering agents or colchicine to statin has been shown to result in additional cardiovascular benefits for patients with atherosclerotic cardiovascular diseases (ASCVD). We aimed to compare the efficacy and safety of these supplementary agents in patients with ASCVD receiving statin.</p><p><strong>Methods: </strong>We performed a systematic review and frequentist network meta-analysis of randomized controlled trials. The primary efficacy endpoint was the main adverse cardiovascular event (MACE), and the secondary efficacy endpoints were myocardial infarct, stroke, coronary revascularization, cardiovascular death, and all-cause mortality, respectively. The safety endpoints were treatment discontinuation and non-cardiovascular death. We obtained estimates for efficacy outcomes and safety endpoints and presented these estimates as risk ratio (RR) with 95% confidence intervals. We ranked the comparative efficacy and safety of all drugs with P-scores.</p><p><strong>Results: </strong>Seventeen trials totaling 85,823 participants treated with colchicine (5926 participants), intensive LDL-C lowering (37,854 participants) via proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitor, Niemann-Pick C1-like 1 protein (NPC1L1) inhibitor or ATP citrate lyase (ACL) inhibitor, or statin alone (42,043 participants) were included. Colchicine was associated with a greater reduction in the risk of MACE (RR 0.72, 0.69-0.91), stroke (RR 0.55, 0.33-0.92), and coronary revascularization (RR 0.73, 0.60-0.90) compared with NPC1L1 inhibitor, and it provided a larger reduction in the risk of MACE (RR 0.79, 0.69-0.91) compared to PCSK9 inhibitor. However, colchicine was associated with increased risk of non-cardiovascular death compared with NPC1L1 inhibitor (RR 1.48, 1.04-2.10) and PCSK9 inhibitor (RR 1.57, 1.08-2.27). Although no regimen prolonged survival, colchicine had worse performance on non-cardiovascular death and all-cause mortality.</p><p><strong>Conclusions: </strong>In patients with ASCVD receiving statin, colchicine seems to be more effective than intensive LDL-C-lowering therapy with PCSK9 inhibitor or NPC1L1 inhibitor for cardiovascular prevention. However, using colchicine as an alternative to intensive LDL-C-lowering therapy may need to be weighed against the cardiovascular benefits and the potential harms of higher non-cardiovascular death.</p><p><strong>Trial registration: </strong>PROSPERO Identifier: CRD42023441385.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"811-822"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142104706","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":"LncRNA Gm15834 Aggravates Cardiac Hypertrophy by Interacting with Sam68 and Activating NF-κB Mediated Inflammation.","authors":"Yongsheng Liu, Man Jiang, Meitian Zhang, Yawen Xie, Lixin Wang, Pilong Shi, Qianlong Zhang, Qianhui Zhang, Kai Liu, Jiajun Zhou, Chao Song, Hongli Sun","doi":"10.1007/s10557-024-07569-x","DOIUrl":"10.1007/s10557-024-07569-x","url":null,"abstract":"<p><strong>Background: </strong>Cardiac hypertrophy is the common pathological process of multiple cardiovascular diseases. However, the molecular mechanisms of cardiac hypertrophy are unclear. Long non-coding RNA (lncRNA), a newly discovered type of transcript that has been demonstrated to function as crucial regulators in the development of cardiovascular diseases. This study revealed a novel regulatory pathway of lncRNA in cardiac hypertrophy.</p><p><strong>Methods: </strong>The cardiac hypertrophy models were established by transverse aortic constriction (TAC) in mice and angiotensin II (Ang II) in HL-1 cardiomyocytes. Adeno-associated virus 9 (AAV9) in vivo and lncRNA Gm15834 and shRNA plasmids in vitro were used to overexpress and knock down lncRNA Gm15834. The myocardial tissue structure, cardiomyocyte area, cardiac function, protein expressions, and binding of lncRNA Gm15834 and Src-associated substrate during mitosis of 68 KDa (Sam68) were detected by hematoxylin and eosin (HE) staining, immunofluorescence staining, echocardiography, western blot and RNA immunoprecipitation (RIP), respectively.</p><p><strong>Results: </strong>In cardiac hypertrophy models, inhibiting lncRNA Gm15834 could decrease Sam68 expression and nuclear factor kappa-B (NF-κB) mediated inflammatory activities in vivo and in vitro, but overexpressing lncRNA Gm15834 showed the opposite results. RIP experiments validated the binding activities between lncRNA Gm15834 and Sam68. Overexpression of Sam68 could counteract the anti-hypertrophy effects of lncRNA Gm15834 knockdown. Meanwhile, in vivo inhibition of lncRNA Gm15834 could inhibit Sam68 expression, reduce NF-κB mediated inflammatory activity and attenuate cardiac hypertrophy.</p><p><strong>Conclusion: </strong>Our study revealed a novel regulatory axis of cardiac hypertrophy, which comprised lncRNA Gm15834/Sam68/NF-κB/inflammation, shedding a new light for identifying therapy target of cardiac hypertrophy in clinic.</p>","PeriodicalId":9557,"journal":{"name":"Cardiovascular Drugs and Therapy","volume":" ","pages":"749-763"},"PeriodicalIF":3.1,"publicationDate":"2025-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140875862","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}