Journal of molecular and cellular cardiology最新文献

{"title":"Corrigendum to “Atrial fibrillation in cancer, anticancer therapies, and underlying mechanisms” [Journal of Molecular and Cellular Cardiology. 194 (2024): 118–132]","authors":"Adnan Shaaban , Shane S. Scott , Ashley N. Greenlee , Nkongho Binda , Noor Ali , Averie Webb , Shuliang Guo , Najhee Purdy , Nicholas Pennza , Alma Habib , Somayya J. Mohammad , Sakima A. Smith","doi":"10.1016/j.yjmcc.2025.06.010","DOIUrl":"10.1016/j.yjmcc.2025.06.010","url":null,"abstract":"","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"205 ","pages":"Page 99"},"PeriodicalIF":4.9,"publicationDate":"2025-07-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144563945","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Mitochondrial thioredoxin-2 maintains HCN4 expression and prevents oxidative stress-mediated sick sinus syndrome” [Journal of Molecular and Cellular Cardiology 138 (2020) 291–303]","authors":"Bicheng Yang , Yanrui Huang , Haifeng Zhang , Yan Huang , Huanjiao Jenny Zhou , Lawrence Young , Haipeng Xiao , Wang Min","doi":"10.1016/j.yjmcc.2025.06.007","DOIUrl":"10.1016/j.yjmcc.2025.06.007","url":null,"abstract":"","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"205 ","pages":"Page 85"},"PeriodicalIF":4.9,"publicationDate":"2025-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144523395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Calcium binding to troponin C is required for activation of the myosin-containing thick filaments in rat cardiac trabeculae","authors":"Michaeljohn Kalakoutis ,&nbsp;Yanhong Wang ,&nbsp;Emma Smith ,&nbsp;Alice Arcidiacono ,&nbsp;Cameron Hill ,&nbsp;Samina Juma ,&nbsp;Atsuki Fukutani ,&nbsp;Elisabetta Brunello ,&nbsp;Luca Fusi ,&nbsp;Malcolm Irving","doi":"10.1016/j.yjmcc.2025.06.012","DOIUrl":"10.1016/j.yjmcc.2025.06.012","url":null,"abstract":"<div><div>Contraction of the muscular walls of the heart is driven by an interaction between myosin motors from the thick filaments and actin sites in the thin filaments. Each heartbeat is triggered by calcium binding to troponin in the thin filaments, which unblocks the myosin-binding sites on actin. The strength and speed of contraction is also modulated by the availability of myosin motors, which are sequestered in a helical array on the surface of the thick filaments between heartbeats. The signalling pathway controlling release of the motors from this array during the heartbeat is unknown, but there are three general hypotheses: thick-filament mechano-sensing, thin-to-thick filament signalling, and direct calcium signalling to the thick filament. Here we tested the third hypothesis by replacing the native calcium-binding subunit of troponin (TnC) with a variant which cannot bind calcium. Demembranated trabeculae from rat heart containing this variant generated no active force on addition of calcium. We measured calcium-induced release of myosin motors from the sequestered state by X-ray diffraction and from the orientation of fluorescent probes on the myosin regulatory light chain. Both methods showed the expected calcium-dependent changes in the conformation of the myosin motors in trabeculae containing native TnC, but all these changes were abolished in those containing the TnC variant that cannot bind calcium. We conclude that thick filament activation in rat heart trabeculae is not due to direct binding of calcium to thick filaments, but is mediated by calcium activation of the thin filaments by mechano-sensing or thin-to-thick filament signalling.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"205 ","pages":"Pages 129-138"},"PeriodicalIF":4.9,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144560419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intermedin1–53 improves aging-associated cardiac remodeling and dysfunction via mitochondrial SIRT3-mediated SOD2 deacetylation","authors":"Deng-Ren Ji ,&nbsp;Rui Chang ,&nbsp;Shi-Meng Liu ,&nbsp;Ya-Rong Zhang ,&nbsp;Jie Zhao ,&nbsp;Yan-Rong Yu ,&nbsp;Mo-Zhi Jia ,&nbsp;Ning Wu ,&nbsp;Hui-Fang Tang ,&nbsp;Chao-Shu Tang ,&nbsp;Ye-Bo Zhou ,&nbsp;Yong-Fen Qi","doi":"10.1016/j.yjmcc.2025.06.011","DOIUrl":"10.1016/j.yjmcc.2025.06.011","url":null,"abstract":"<div><div>The aging-associated cardiac remodeling (AACR) is characterized by myocardial hypertrophy, fibrosis and cardiac dysfunction, which could be further aggravated by angiotensin II (Ang II) and pressure-overload in aged people. In this study, we aimed to investigate the roles and mechanisms of intermedin₁_–₅₃ (IMD₁_–₅₃), an endogenous peptide, in AACR in aged mice (18 months) with subcutaneous Ang II infusion (1000 ng/kg/min) for 2 weeks via osmotic pump or transverse abdominal aorta constriction (AAC) surgery for 4 weeks. In aged mice undergoing Ang II infusion or AAC surgery, the results showed that the mRNA and protein levels of IMD₁_–₅₃ were significantly reduced, but the protein levels of its receptor complex components were increased; blood pressure (BP), myocardial hypertrophy, fibrosis, and cardiac dysfunction were notably aggravated; mitochondrial Sirtuin 3 (SIRT3) protein level, superoxide dismutase 2 (SOD2) activity and ATP production were remarkably decreased, but acetylated SOD2 (acSOD2) protein level was markedly increased when compared with the old mice. The above alterations could be effectively alleviated by the subcutaneous IMD₁_–₅₃ administration (5 ng/kg/min) for 2 or 4 weeks. In Ang II-stimulated cardiomyocytes, IMD₁_–₅₃ treatment improved Ang II-induced mitochondrial dysfunction and oxidative distress, up-regulated SIRT3 protein expression, and reduced acSOD2 protein level, which were notably weakened by SIRT3 knockdown. Moreover, SIRT3 deletion attenuated the protective effects of IMD₁_–₅₃ on myocardial hypertrophy, fibrosis, and cardiac dysfunction in aged mice undergoing Ang II infusion. In addition, the effect of IMD₁_–₅₃ on up-regulating SIRT3 expression was effectively inhibited by the antagonism of IMD₁_–₅₃ receptor or blocking PI3K/Akt, cAMP/PKA and AMPK signaling pathways in vitro. Taken together, IMD₁_–₅₃ alleviated AACR and cardiac dysfunction aggravated by Ang II or pressure-overload involving the improvement of mitochondrial oxidative distress through SIRT3-medaiated SOD2 deacetylation.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"205 ","pages":"Pages 86-98"},"PeriodicalIF":4.9,"publicationDate":"2025-06-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144548388","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Corrigendum to “Hypoxic compound exercise improves cardiac function in Drosophila high fructose diet via KHK” [Journal Of Molecular And Cellular Cardiol. 201(2025):95–104]","authors":"Xu Ping,&nbsp;Qiufang Li,&nbsp;Meng Ding,&nbsp;Zhengwen Yu,&nbsp;Qin Yi,&nbsp;Yuepeng Li,&nbsp;Wenzhi Gu,&nbsp;Ping Zhang,&nbsp;Zike Zhang,&nbsp;Lan Zheng","doi":"10.1016/j.yjmcc.2025.06.006","DOIUrl":"10.1016/j.yjmcc.2025.06.006","url":null,"abstract":"","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"205 ","pages":"Page 84"},"PeriodicalIF":4.9,"publicationDate":"2025-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144502171","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular mechanism for the interaction of MOG1 with the intracellular loop II of cardiac sodium channel Nav1.5 and its role in arrhythmias","authors":"Xuemei Bai ,&nbsp;Zhijie Wang ,&nbsp;Hongbo Xiong ,&nbsp;Chipeng Yan ,&nbsp;Yufeng Yao ,&nbsp;Chengqi Xu ,&nbsp;Hui Li ,&nbsp;Qing K. Wang","doi":"10.1016/j.yjmcc.2025.06.005","DOIUrl":"10.1016/j.yjmcc.2025.06.005","url":null,"abstract":"<div><div><em>SCN5A</em> encodes the cardiac sodium channel α-subunit Na_v1.5, and its variants cause long QT syndrome (LQTS), Brugada syndrome (BrS) and other arrhythmias. MOG1 interacts with Na_v1.5 to increase cardiac sodium current densities, however, molecular mechanisms remain poorly defined. The objectives of this study were to identify the crucial structural elements responsible for the interaction between MOG1 and Na_v1.5 intracellular Loop II, and determine the significance of this interaction to cardiac arrhythmias. Whole-cell patch-clamping was used to record sodium current <em>I</em>_<em>Na</em> in tsA201 and neonatal rat primary cardiomyocytes. Glutathione S-transferase (GST) pull-down assays were used to characterize protein-protein interactions. Mutagenesis was used to create deletions and point mutations. Characterization of large deletions and small deletions of Na_v1.5 Loop II 940–1200 defined the MOG1-interacting domain to V₁₁₉₀-H₁₂₀₀. Point mutation analysis revealed that amino acids R₁₁₉₅, Y₁₁₉₉ and H₁₂₀₀ were involved in MOG1-Na_v1.5 Loop II interaction. Two variants of MOG1-interacting domain from human patients showed important functional effects. Variant p.R1195C was identified in two individuals with cardiac arrhythmias in ClinVar, weakened the interaction between Na_v1.5 and MOG1, and reduced MOG1-enhanced cardiac sodium current densities. Variant p.Y1199S was identified in one individual with LQTS and one with cardiac arrhythmias, generated late <em>I</em>_<em>Na</em>, weakened the interaction between Na_v1.5 and MOG1, and reduced MOG1-enhanced cardiac sodium current densities. This study identifies three critical amino acids R₁₁₉₅, Y₁₁₉₉ and H₁₂₀₀ of Na_v1.5 Loop II for interaction with MOG1, and reveals the molecular mechanisms by which variants p.R1195C and p.Y1199S in MOG1-interacting domain cause LQTS and cardiac arrythmias.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"205 ","pages":"Pages 68-83"},"PeriodicalIF":4.9,"publicationDate":"2025-06-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144340209","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of FoxO1 prevents and reverses cardiac hypertrophy from diverse stimuli","authors":"Thomas G. Martin ,&nbsp;Stephen J. Langer ,&nbsp;Claudia Crocini ,&nbsp;Eunhee Chung ,&nbsp;Leslie A. Leinwand","doi":"10.1016/j.yjmcc.2025.06.008","DOIUrl":"10.1016/j.yjmcc.2025.06.008","url":null,"abstract":"<div><div>The heart is a dynamic organ capable of structural and functional remodeling in the wake of changing mechanical and/or circulating cues. While the molecular underpinnings of cardiac hypertrophy are well-defined, the mechanisms of hypertrophy regression following stimulus removal are relatively less understood. Here, we demonstrate that activation of forkhead box proteins (FoxOs), and increased expression of their autophagy gene targets, are common features of hypertrophy regression after both exercise and pregnancy in mice. Additionally, we show FoxO1 activation is sufficient to prevent and reverse adrenergic agonist-dependent pathological hypertrophy. Our findings highlight the central role of FoxO1 in regulating cardiac mass.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"205 ","pages":"Pages 62-67"},"PeriodicalIF":4.9,"publicationDate":"2025-06-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144321735","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Endothelial CD36 mediates diet-induced increases in aortic stiffness","authors":"Javad Habibi ,&nbsp;Vincent G. DeMarco ,&nbsp;Dongqing Chen ,&nbsp;Adam Whaley-Connell ,&nbsp;Michael A. Hill ,&nbsp;Guanghong Jia","doi":"10.1016/j.yjmcc.2025.06.009","DOIUrl":"10.1016/j.yjmcc.2025.06.009","url":null,"abstract":"<div><div>A Western diet (WD) contributes to the rising prevalence of obesity and insulin resistance, both of which are key risk factors for arterial stiffening and related cardiovascular diseases. We recently found that elevated CD36 is associated with increased ectopic lipid accumulation, systemic and tissue insulin resistance, and arterial stiffening. Here, we further examined whether endothelial cell (EC) specific CD36 (ECCD36) participates in WD-induced aortic insulin resistance, lipid accumulation, inflammation, fibrosis, remodeling, and associated aortic stiffening. Female ECCD36 knockout (ECCD36^−/−) and wild-type (ECCD36^+/+) mice, at six weeks of age, were fed either a Western diet (WD) or a standard chow diet (CD) for 16 weeks. Aortic stiffness and activity were investigated by ultrasound (pulse wave velocity) and wire myography, respectively. Gene expression was monitored by western blot and quantitative PCR. Lipid content and aortic remodeling were explored by Oil red O staining and immunostaining, respectively. 16 weeks of WD increased aortic stiffening that was associated with vascular insulin resistance and reduced insulin metabolic signaling via phosphoinositide 3-kinases/protein kinase B. The pathophysiological changes in vascular insulin resistance and stiffening were associated with activation of mammalian target of rapamycin/S6 kinase signaling, increased lipid disorders, decreased tight junction-associated protein occludin, and increased proinflammatory response, and aortic remodeling. These abnormalities were blunted in ECCD36^−/− mice fed a WD. These findings suggest that under an obesogenic Western diet (WD), heightened ECCD36 signaling contributes to aortic insulin resistance, increased lipid accumulation, increased endothelial permeability and proinflammatory responses, fibrosis, vascular remodeling, and consequent aortic stiffening.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"205 ","pages":"Pages 52-61"},"PeriodicalIF":4.9,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144307138","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Mechanisms underlying atrial fibrillation in chronic kidney disease","authors":"Jose Alberto Navarro-Garcia ,&nbsp;Joshua A. Keefe ,&nbsp;Jia Song ,&nbsp;Na Li ,&nbsp;Xander H.T. Wehrens","doi":"10.1016/j.yjmcc.2025.06.002","DOIUrl":"10.1016/j.yjmcc.2025.06.002","url":null,"abstract":"<div><div>Chronic kidney disease (CKD) is a serious and progressive worldwide health problem affecting 15 % of the global population. CKD is associated with higher mortality rates due to secondary complications such as cardiovascular disease. Common cardiovascular complications found in CKD patients include left ventricular hypertrophy, heart failure, and cardiac arrhythmias. The most common type of cardiac arrhythmia in CKD patients is atrial fibrillation (AF). Proper management of AF is important due to its high risk of cardiovascular complications and stroke. The incidence of AF remains higher in CKD patients than in the healthy population, highlighting the need to improve our understanding of the mechanisms underlying CKD-induced AF. In this review, we discuss well-known systemic factors linking CKD to AF pathogenesis. We highlighted the involvement of several inflammatory mediators in the CKD-induced atrial arrhythmogenesis. We also address special considerations for experimental models of CKD and AF management in CKD patients. Finally, we emphasize the need for a deeper understanding of the molecular underpinning, and for high-quality clinical investigations into the CKD-AF connection.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"205 ","pages":"Pages 37-51"},"PeriodicalIF":4.9,"publicationDate":"2025-06-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144272183","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Optogenetic mitochondrial preconditioning enhances cardiomyocyte survival under stress","authors":"Seulhee Kim ,&nbsp;Hwayeon Lim ,&nbsp;Patrick Ernst ,&nbsp;Li Zhu ,&nbsp;Jiashuai Zhang ,&nbsp;Min Xie ,&nbsp;Xiaoguang “Margaret” Liu ,&nbsp;Lufang Zhou","doi":"10.1016/j.yjmcc.2025.06.004","DOIUrl":"10.1016/j.yjmcc.2025.06.004","url":null,"abstract":"<div><div>Mitochondria play a central role in preconditioning-mediated cytoprotection, yet the specific role of mitochondrial membrane potential (ΔΨ_m) in this process remains incompletely understood. In this study, we employed a next-generation, mitochondrial-targeted optogenetic system (mOpto) to induce precisely controlled (partial and transient) ΔΨ_m depolarization and investigate its role in enhancing cardiomyocyte resilience to stress. Human AC16 cardiomyocytes expressing mOpto were subjected to low-intensity LED illumination for preconditioning, followed by exposure to stressors including FCCP, H₂O₂, or simulated ischemia-reperfusion. mOpto-preconditioned cells exhibited significantly improved viability, attenuated ΔΨ_m depolarization, and reduced reactive oxygen species (ROS) production compared to non-preconditioned controls. Notably, this cytoprotective effect occurred independently of canonical ROS signaling and mitochondrial ATP-sensitive potassium channel (mitoK_ATP) activation. Transcriptional analysis revealed coordinated mitochondrial and metabolic reprogramming, including upregulation of genes involved in lipid biosynthesis, mitochondrial quality control, energy homeostasis, and a shift toward mitochondrial fusion. Importantly, mOpto preconditioning conferred similar cytoprotective effects in human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), underscoring the translational potential of this approach. These findings demonstrate that mOpto-mediated transient ΔΨ_m depolarization induces a preconditioning effect that enhances cardiomyocyte resilience through the establishment of a mitochondrial “memory” and dynamic remodeling of mitochondrial function.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"205 ","pages":"Pages 24-36"},"PeriodicalIF":4.9,"publicationDate":"2025-06-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144263399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}