Journal of molecular and cellular cardiology plus最新文献

{"title":"Dysregulation of lncRNA IRENE Disrupts Endothelial-Cardiomyocyte Interactions: New Insights into the Molecular Mechanisms of HFpEF","authors":"Rio Juni , Carla Cofino-Fabres , Lily Jalink , Elisa Osei-Bonsu , Philippa Phelp , Judith Ponce , Anke van Bergen , Caroline Janssen , Louis Handoko , Matthias Leissegang , Ralf Brandes , Robert Passier , Reinier Boon","doi":"10.1016/j.jmccpl.2025.100566","DOIUrl":"10.1016/j.jmccpl.2025.100566","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"15 ","pages":"Article 100566"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147538760","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive Profiling of Isoform Dynamics in Heart Maturation","authors":"Woan Ting Tay , Jia Li , Jijun Huang , Lei Sun , Yibin Wang","doi":"10.1016/j.jmccpl.2025.100567","DOIUrl":"10.1016/j.jmccpl.2025.100567","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"15 ","pages":"Article 100567"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147538761","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thymic Activity Modulates Immune Checkpoint Inhibitor-Induced Cardiotoxicity: Implications for Therapeutic Strategies","authors":"Marton Kocsis , Anna Kulin , Lilla Szabo , Tamas Gergely , Viktor Nabil Sayour , Viktoria Toth , Luca Varga , David Nagy , Tamas Kovacs , Barnabas Varadi , Zoltan Varga","doi":"10.1016/j.jmccpl.2025.100586","DOIUrl":"10.1016/j.jmccpl.2025.100586","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"15 ","pages":"Article 100586"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147536723","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Generation of a Novel Constitutive Smooth Muscle Cell-Specific Myh11-driven Cre Mouse Model","authors":"Kunzhe Dong , Zhixia Bai , Xiangqin He , Lu Zhang , Guoqing Hu , Yali Yao , Chen-Leng Cai , Jiliang Zhou","doi":"10.1016/j.jmccpl.2025.100574","DOIUrl":"10.1016/j.jmccpl.2025.100574","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"15 ","pages":"Article 100574"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147537924","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Disclaimer","authors":"","doi":"10.1016/S2772-9761(26)00008-5","DOIUrl":"10.1016/S2772-9761(26)00008-5","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"15 ","pages":"Article 100841"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147538059","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNA modifications in peripheral blood are associated with acute coronary syndrome","authors":"Miron Sopic ,&nbsp;Victoria Stopa ,&nbsp;Jelena Munjas ,&nbsp;Aleksandar Davidović ,&nbsp;Luka Vukmirović ,&nbsp;Dane Cvijanović ,&nbsp;Marko Milanov ,&nbsp;Fabio Martelli ,&nbsp;François Bernardin ,&nbsp;Nathalie Michelle Legrave ,&nbsp;Yvan Devaux","doi":"10.1016/j.jmccpl.2026.100839","DOIUrl":"10.1016/j.jmccpl.2026.100839","url":null,"abstract":"<div><div>Acute coronary syndromes (ACS) trigger inflammatory and immune reactions, yet whether this response is associated with changes in RNA modifications remains poorly understood. We investigated global epitranscriptomic patterns in peripheral blood mononuclear cells (PBMC) from patients with ST-elevation myocardial infarction (STEMI, <em>n</em> = 118), non-ST-elevation myocardial infarction (NSTEMI, <em>n</em> = 22), unstable angina pectoris (UAP, <em>n</em> = 10), and stable angina pectoris (SAP, <em>n</em> = 152). Using liquid chromatography–mass spectrometry, we quantified N1-methyladenosine (m1A), 2′-<em>O</em>-methyladenosine (2′-O-mA), N6-methyladenosine (m6A), N6,2′-<em>O</em>-dimethyladenosine (m6Am), and pseudouridine (Ψ), together with their ratios to unmodified nucleotides.</div><div>Levels of 2′-O-mA (<em>P</em> = 0.004), m6Am (<em>P</em> &lt; 0.001), and Ψ (<em>P</em> = 0.021) were significantly decreased in STEMI compared with SAP. m6Am was also reduced in UAP (<em>P</em> = 0.037) and NSTEMI (<em>P</em> = 0.012), whereas m1A and m6A did not differ between groups. Among modification ratios, only the m6Am/A ratio declined across ACS subtypes (UAP <em>P</em> = 0.015; NSTEMI <em>P</em> = 0.032; STEMI <em>P</em> = 0.007), indicating relative cap-adjacent hypomethylation. Reduced m6Am correlated inversely with hsCRP (<em>r</em> = −0.19, P &lt; 0.001) and hsTnI (<em>r</em> = −0.24, P &lt; 0.001). In multivariable logistic regression adjusting for age, sex, BMI, and hsCRP, m6Am remained independently associated with STEMI (OR = 0.14, 95% CI 0.02–0.81; <em>P</em> = 0.028).</div><div>These findings demonstrate selective RNA modification changes in ACS and identify m6Am as an independent epitranscriptomic marker associated with myocardial infarction.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"15 ","pages":"Article 100839"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147395612","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"SARS-CoV-2-infected cardiomyocytes exhibit upregulated necroptosis, but no evidence of mitochondrial permeability transition","authors":"C. Gross ,&nbsp;S. Chatterjee ,&nbsp;B.E. Nilsson-Payant ,&nbsp;S.D. Stojanović ,&nbsp;H. Kefalakes ,&nbsp;C. Bär ,&nbsp;T. Thum ,&nbsp;T. Pietschmann ,&nbsp;J. Bauersachs ,&nbsp;G. Amanakis","doi":"10.1016/j.jmccpl.2025.100833","DOIUrl":"10.1016/j.jmccpl.2025.100833","url":null,"abstract":"<div><div>Cardiac involvement in patients infected with COVID-19, in terms of myocarditis and troponin release, is associated with higher mortality. However, the underlying mechanisms are poorly understood.</div><div>Infection of cardiomyocytes derived from human induced pluripotent stem cells (iPSC-CMs) with a wild-type variant of SARS-CoV-2 exhibited a cardiotoxic effect. We examined whether elevated intramitochondrial calcium causes opening of the mitochondrial permeability transition pore (mPTP) leading to cell death. The mPTP inhibitor Cyclosporine A (CsA) did not improve viability, and phosphorylation levels of pyruvate dehydrogenase (PDH) remained similar pre- and post-infection, likely suggesting no substantial alteration of the intramitochondrial calcium level. Also, the protein expression of mitochondrial respiratory complexes did not change after SARS-CoV-2 infection.</div><div>Next, we examined whether cell death is related to necroptosis or pyroptosis upregulation. The phosphorylation level of receptor-interacting protein kinase 3 (RIP3) was elevated post-infection with SARS-CoV-2 while phosphorylation of mixed lineage kinase domain (MLKL)-S358 remained unaltered. This pattern may point toward an alternative regulation of necroptosis. Chemical inhibition of necroptosis (Necrostatin-1) and pyroptosis (MCC950) did not confer any protection. Notably, the phosphorylation of RIP3 under Necrostatin-1 was still elevated, suggesting that autophosphorylation of RIP3 may be a possible confounder.</div><div>Our data suggest that SARS-CoV-2 compromises cell viability in iPSC-CMs and may engage in non-canonical signaling via RIP3 phosphorylation. The lack of MLKL activation and the absence of protective effects from CsA indicate that neither classical necroptosis nor mitochondrial permeability transition are likely to be central regulators of cell death.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"15 ","pages":"Article 100833"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145926551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A perspective on the future of heart failure research","authors":"Alyssa C. Vadovsky ,&nbsp;Eunji Jeong ,&nbsp;Sandeep Banga ,&nbsp;Jason N. Bazil","doi":"10.1016/j.jmccpl.2026.100835","DOIUrl":"10.1016/j.jmccpl.2026.100835","url":null,"abstract":"<div><div>Heart failure is chronic condition that is diagnosed when the heart is no longer able to pump enough blood to meet the physiological needs of the body. It is a progressive condition and typically manifests early on as exercise intolerance due to insufficient cardiac output before developing into the end stage disease. Nearly 7 million U.S. adults currently live with some form of heart failure, roughly accounting for 14% of all deaths. Various etiologies of heart failure have been identified which stem from a constellation of perfusion, pressure, morphological, electrical, and/or metabolic origins. An underlying issue for nearly all forms of heart failure is what is known as bioenergetic abnormalities. Although mitochondrial dysfunction is widely implicated, the precise molecular mechanisms underlying bioenergetic abnormalities remain incompletely understood. In this commentary, we describe the most prevalent heart failure types and offer a possible mechanism capable of explaining these bioenergetic abnormalities. We explore a novel hypothesis that links oxidative stress caused by intrinsic and extrinsic factors, which leads to depressed oxidative capacities induced by the presence of mitochondrial calcium phosphate granules. This hypothesis is supported by evidence previously reported in literature and may offer a new etiology of heart failure. We conclude by outlining a bold strategy to advance heart failure research through innovative approaches and unexplored domains.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"15 ","pages":"Article 100835"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146173633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistently increased CaMKIIδ autophosphorylation mediates pathologic SR Ca loss in a murine model of Doxorubicin-induced cardiomyopathy","authors":"Anna-Lena Feder ,&nbsp;Daniel Tarnowski ,&nbsp;Anna-Maria Pfützenreuter ,&nbsp;Maria Johanna Baier ,&nbsp;Julian Mustroph ,&nbsp;Maithily S. Nanadikar ,&nbsp;Dörthe M. Katschinski ,&nbsp;Lars Siegfried Maier ,&nbsp;Can Martin Sag","doi":"10.1016/j.jmccpl.2025.100828","DOIUrl":"10.1016/j.jmccpl.2025.100828","url":null,"abstract":"<div><h3>Background</h3><div>Doxorubicin (DOX)-induced cardiomyopathy (DICM) manifests as left ventricular (LV) systolic dysfunction. DOX triggers oxidative stress and CaMKIIδ activity in cardiac myocytes. CaMKIIδ activation leads to impaired intracellular Ca handling and contractile dysfunction because of pathologic Ca loss from the sarcoplasmic reticulum (SR). While CaMKIIδ is canonically activated by autophosphorylation, it can also be activated via oxidation.</div></div><div><h3>Objectives</h3><div>We aimed to investigate the <em>predominant</em> mode of CaMKIIδ activation in DICM.</div></div><div><h3>Methods</h3><div>We utilized two transgenic mouse models, one lacking CaMKIIδ (CaMKIIδ^−/−) and a “redox-dead” CaMKIIδ^Val281/282 model. Acute changes in intracellular Ca handling and CaMKIIδ activation status were examined following 15 min of DOX exposure. Long-term effects were studied in CaMKIIδ^−/− mice (vs. CaMKIIδ^+/+ wildtype littermates) and redox-dead CaMKIIδ^Val281/282 mice (vs. CaMKIIδ^Met281/282 wildtype littermates) that underwent DOX treatment in-vivo. Cardiac function (via echocardiography), intracellular Ca handling, and CaMKIIδ-related signaling were assessed 12 weeks post-treatment.</div></div><div><h3>Results</h3><div>DOX <em>acutely</em> increased CaMKIIδ activity by autophosphorylation <em>and</em> oxidation in both WT lines, while autophosphorylated CaMKIIδ was still detected in CaMKIIδ^Val281/282 mice, which resulted in comparably increased SR Ca leakage mediated by CaMKII-dependent RyR2-hyperphosphorylation at pS2814 in all aforementioned groups. In contrast, pharmacological and genetic inhibition of CaMKIIδ (i.e. in CaMKIIδ^−/−) prevented DOX-induced CaMKIIδ-hyperactivation, RyR2-hyperphosphorylation and SR Ca loss. Similarly, only CaMKIIδ^−/− mice were protected from long-term DOX-induced LV dysfunction in-vivo. Redox-dead CaMKIIδ^Val281/282 mice exhibited similar LV dysfunction as WT littermates, with persistent CaMKIIδ autophosphorylation, subsequent RyR2 hyperphosphorylation, and increased CaMKIIδ-dependent SR Ca leakage.</div></div><div><h3>Conclusions</h3><div>Persistently increased CaMKIIδ autophosphorylation, but not oxidation, mediates pathologic SR Ca loss in Doxorubicin-induced cardiomyopathy.</div></div>","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"15 ","pages":"Article 100828"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145665349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Synergy effects of extracellular vesicles from human embryonic stem cells and their-derived cardiac lineage cells in cardiac repair","authors":"Qiang Wu ,&nbsp;Xiujian Yu ,&nbsp;Minxia Ke ,&nbsp;Shihui Wang ,&nbsp;Hao Li ,&nbsp;Peng Zhang ,&nbsp;Huang-Tian Yang","doi":"10.1016/j.jmccpl.2025.100532","DOIUrl":"10.1016/j.jmccpl.2025.100532","url":null,"abstract":"","PeriodicalId":73835,"journal":{"name":"Journal of molecular and cellular cardiology plus","volume":"15 ","pages":"Article 100532"},"PeriodicalIF":2.2,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147536738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}