Journal of molecular and cellular cardiology最新文献

{"title":"Myofibroblast specific knockdown of NSUN2 suppresses cardiac fibrosis post-myocardial infarction.","authors":"Zhiyong Sun, Na Li, Min Huang, Ying Li, Changhao Wang, Zhezhe Qu, Shuting Yu, Zhongting Mei, Bo Wu, Shunkang Dou, Jianhao Jiang, Yaozhi Zhang, Chuanhao Huang, Jiaqi Han, Yufei Yue, Xin Li, Yuechao Dong, Weijie Du","doi":"10.1016/j.yjmcc.2025.09.009","DOIUrl":"https://doi.org/10.1016/j.yjmcc.2025.09.009","url":null,"abstract":"<p><p>Cardiac fibrosis, a common pathological process characterized by excessive deposition of extracellular matrix components in the myocardium, poses a critical challenge in the field of cardiovascular research and clinical practice. 5-Methylcytosine (m5C) is an extensive post-transcriptional RNA modification known to participate in various cellular responses and biological processes by regulating RNA metabolism. However, it remains unclear whether m5C RNA modifications exert regulatory effects on cardiovascular diseases, particularly cardiac fibrosis. Here, we report that NSUN2, a typical m5C methyltransferase, affects the RNA stability of HuR through m5C modification, promoting the development of cardiac fibrosis. Upon the conditional knockdown of NSUN2 specifically in myofibroblasts, the extent of cardiac fibrosis was suppressed. In conclusion, we specifically knocked down NSUN2 in cardiac myofibroblasts, which further reduced the RNA stability of HuR and thus ameliorated cardiac fibrosis caused by myocardial ischemia, offering a new therapeutic target for the clinical treatment of cardiac fibrosis.</p>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-10-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145228419","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":"Animal models and mechanisms of exercise in attenuating cardiac injury induced by beta-adrenergic hyperactivation","authors":"Yong Peng ,&nbsp;Linlin Shang ,&nbsp;Gan Chen ,&nbsp;Simeng Zhao ,&nbsp;Mengyun Mao ,&nbsp;Danxi Zhu ,&nbsp;Di Qin","doi":"10.1016/j.yjmcc.2025.09.007","DOIUrl":"10.1016/j.yjmcc.2025.09.007","url":null,"abstract":"<div><div>Acute sympathetic stress, which causes hyperactivation of β-adrenergic receptors (β-AR) in the heart, is a key pathological factor in the development of cardiac disease. Isoproterenol (ISO) is a non-selective β-AR agonist, which was utilized to develop an experimental animal model of pathological cardiac remodeling, simulating the acute sympathetic stress-induced cardiac injury. Current research evidences support the potential role of exercise in preventing or treating heart injury caused by β-adrenergic overactivation. The mechanisms of exercise against ISO-induced cardiac injury include of inhibiting cardiac inflammation and oxidative stress, suppressing apoptosis, pyroptosis, and necroptosis in cardiomyocytes, activating Adenosine 5′ -monophosphate (AMP)-activated protein kinase (AMPK) signaling pathway, reducing reactive oxygen species (ROS) to regulate the inflammatory response. Despite the protective effects of exercise in attenuating ISO-induced cardiac injury, further studies are necessary to explore the optimal combination of exercise intensity and duration. Additionally, comparative research is required to evaluate the protective effects of different exercise types, investigate the relationship between exercise-induced protection and ISO dosage, and reveal new mechanism underlying the protective effects of exercise against ISO-induced heart injury. This study will improve our understanding of the mechanisms by which exercise protects against cardiac injury induced by β-adrenergic overload, and establish a stronger foundation for studying the effects of exercise against β-adrenergic overload-induced cardiac injury.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"209 ","pages":"Pages 15-26"},"PeriodicalIF":4.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212821","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":"Decoding long COVID-associated cardiovascular dysfunction: Mechanisms, models, and new approach methodologies.","authors":"Dilip Thomas, Phillip C Yang, Joseph C Wu, Nazish Sayed","doi":"10.1016/j.yjmcc.2025.09.008","DOIUrl":"https://doi.org/10.1016/j.yjmcc.2025.09.008","url":null,"abstract":"<p><p>The COVID-19 pandemic has revealed that the impact of SARS-CoV-2 infection extends well beyond the acute phase, with long-term sequelae affecting multiple organ systems, most notably, the cardiovascular system. Long COVID, or post-acute sequelae of SARS-CoV-2 infection (PASC), is characterized by persistent symptoms such as fatigue, dyspnea, chest pain, and palpitations, which can last for months or even years after initial recovery. Increasing evidence implicates immune dysregulation, endothelial dysfunction, persistent viral antigens, and coagulopathy as central drivers of cardiovascular complications. Mechanistic studies demonstrate that direct viral infection of cardiac and vascular cells, along with autoantibody formation and cytokine-mediated injury, contribute to myocardial inflammation, fibrosis, and arrhythmias. Sex-based immunological differences and underlying comorbidities further influence individual susceptibility and disease trajectory. Large-scale epidemiological studies have confirmed significantly increased risks of pericarditis, cardiomyopathy, dysrhythmias, and heart failure among COVID-19 survivors. In parallel, the emergence of advanced preclinical platforms, including patient-derived induced pluripotent stem cell (iPSC)-based cardiac organoids, engineered heart tissues, and organ-on-a-chip systems has enabled mechanistic dissection of Long COVID pathophysiology. These human-relevant models, when integrated with clinical datasets and artificial intelligence (AI)-driven analytics, offer powerful tools for biomarker discovery, risk stratification, and precision therapeutic development. This review synthesizes the current understanding of cardiovascular involvement in Long COVID, highlights key mechanistic insights from both clinical and preclinical studies, and outlines future directions for diagnostic and therapeutic innovation.</p>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145212785","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":"Targeting the NLRP3 Inflammasome-Gasdermin D Axis to Combat Cardiovascular Diseases","authors":"Judy S. Choi ,&nbsp;Mehnaz Pervin ,&nbsp;James E. Vince ,&nbsp;Arpeeta Sharma ,&nbsp;Judy B. de Haan","doi":"10.1016/j.yjmcc.2025.09.006","DOIUrl":"10.1016/j.yjmcc.2025.09.006","url":null,"abstract":"<div><div>Cardiovascular disease remains a leading global cause of mortality, with inflammation playing a crucial role in driving its pathology. Despite advancements in cardiovascular disease management, current treatment options primarily address risk factors and symptoms rather than underlying disease mechanisms. Among the key mechanistic drivers are the NLRP3 multiprotein inflammasome complexes of the innate immune system, which are activated in response to cellular stress or injury. One of the key downstream effectors of NLRP3 activation is gasdermin D, which forms pores in the plasma membrane to initiate pyroptotic cell death, leading to the release of pro-inflammatory cytokines. This review will highlight the role of NLRP3 inflammasome activation and gasdermin D-mediated pyroptosis in driving cardiovascular diseases, including atherosclerosis, myocardial infarction, ischemic stroke and diabetic cardiomyopathy. It will also identify recent innovative therapeutic approaches that target the NLRP3 inflammasome-gasdermin D axis, which are currently being evaluated in preclinical studies and clinical trials.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"209 ","pages":"Pages 1-14"},"PeriodicalIF":4.7,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145149344","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":"SMYD1-mediated mono-methylation of lysine K35 of sarcomeric myosin heavy chain (MHC) regulates sarcomere assembly and homeostasis in zebrafish and human iPSC-derived cardiomyocytes","authors":"Federica Diofano ,&nbsp;Chidinma Amadi ,&nbsp;Larissa Hartmann ,&nbsp;Bernd M. Gahr ,&nbsp;Karolina Weinmann-Emhardt ,&nbsp;Wolfgang Rottbauer ,&nbsp;Steffen Just","doi":"10.1016/j.yjmcc.2025.09.002","DOIUrl":"10.1016/j.yjmcc.2025.09.002","url":null,"abstract":"<div><div>The SMYD family comprises a distinct class of lysine methyltransferases (KMTases) that methylate both histone and non-histone proteins. Among its five members (SMYD1–5), SMYD1 has been identified as a cardiac and skeletal muscle-specific KMTase that interacts with Myosin, in coordination with Unc45b and Hsp90a, to regulate thick filament assembly. However, the precise mechanism by which SMYD1 orchestrates Myosin assembly remains largely unknown.</div><div>Here, we demonstrate that SMYD1 physically associates with the N-terminal region of several myosin heavy chain (MyHC) isoforms and specifically catalyzes the mono-methylation of MyHC at lysine 35 (K35). Methylated MyHC is correctly incorporated into sarcomeres, whereas unmethylated MyHC in Smyd1-deficient zebrafish undergoes degradation <em>via</em> the ubiquitin-proteasome system (UPS), leading to defective thick filament assembly. Although UPS inhibition with MG132 restores Myosin levels in Smyd1-deficient zebrafish embryos, proper thick filament assembly remains impaired due to the absence of K35 MyHC mono-methylation.</div><div>Similar to zebrafish striated muscle cells, SMYD1-mediated MyHC methylation is essential for thick filament assembly but also homeostasis in human cardiomyocytes, indicating a conserved cross-species mechanism of Myosin regulation, first described nearly 40 years ago. Further research is now required to explore the therapeutic potential of targeting this pathway in cardiomyopathies and skeletal muscle disorders.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"208 ","pages":"Pages 74-84"},"PeriodicalIF":4.7,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091587","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":"Single cell analysis identifies a distinct population of fibroblasts that mediate increased cell-cell communication in murine aortopathy of Loeys-Dietz syndrome","authors":"Sayantan Jana ,&nbsp;Shalabh Shukla ,&nbsp;Nicole Sanford ,&nbsp;Chloe Y. Lee ,&nbsp;Abigail Regan ,&nbsp;Li Liu ,&nbsp;David A. Dichek","doi":"10.1016/j.yjmcc.2025.09.005","DOIUrl":"10.1016/j.yjmcc.2025.09.005","url":null,"abstract":"<div><h3>Background</h3><div>Loeys-Dietz syndrome (LDS), caused by heterozygous loss-of-function mutations in members of transforming growth factor β (TGFβ) pathway, results in frequent aortic root aneurysms and type A dissections in human.</div></div><div><h3>Methods</h3><div>To unveil the mechanism of pathogenesis, the present study utilized single cell RNA sequencing (scRNAseq) from the proximal aortas (aortic root and ascending aorta) of 20 weeks old LDS (<em>Tgfbr2</em>^{<em>G357W/+</em>}) and wild type (<em>Tgfbr2</em>^<em>+/+</em>) mice. Histological and immunofluorescence studies were performed on 30 weeks old mice.</div></div><div><h3>Results</h3><div>ScRNAseq study identifies presence of an exclusive fibroblast population (remodeling fibroblasts) in the proximal aortas of LDS mice, which differentially expressed increased extracellular matrix remodeling genes (<em>Mmp3, Col6a5, Col3a1, and Fn1</em>), and macrophage recruiting chemokines (<em>Saa3, Ccl7, Ccl8, and Cxcl11</em>). These remodeling fibroblasts are focally localized with macrophages at the adventitia of dilated aortic roots of LDS mice. LDS aortas showed increased accumulation of <em>Ccr2</em> expressing infiltrating macrophages, which are functionally involved in phagocytosis, immune responses and antigen processing and presentation. Ligand-receptor based interaction model recognizes remodeling fibroblasts as a major mediator for signaling communications with resident and recruited macrophages in the proximal aortopathies of LDS mice.</div></div><div><h3>Conclusion</h3><div>Our study highlights the presence of a specialized fibroblast population in the dilated aortic roots of LDS mice at 20 weeks and provides a deeper insight for involvement of remodeling fibroblasts in cellular heterogeneity and cell-cell communications in LDS aortopathies.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"208 ","pages":"Pages 60-73"},"PeriodicalIF":4.7,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145091591","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":"Circadian determinants of heart rhythm and arrhythmias","authors":"Mark Boyett ,&nbsp;Pan Li ,&nbsp;Yirong Xiang ,&nbsp;Henggui Zhang ,&nbsp;Jae Kyoung Kim ,&nbsp;Alicia D'Souza","doi":"10.1016/j.yjmcc.2025.08.012","DOIUrl":"10.1016/j.yjmcc.2025.08.012","url":null,"abstract":"<div><div>This review concerns the mechanisms underlying the circadian rhythm in the electrical activity of the healthy heart. Attention is focussed on the circadian rhythm of the heart rate, the PR interval and the vulnerability to ventricular tachyarrhythmias, because they help to explain the circadian rhythm in the incidence of bradyarrhythmias, atrioventricular block, ventricular fibrillation and sudden cardiac death. Ultimately, all cardiac circadian rhythms are assumed to be extracardiac in origin, driven by a master circadian clock in the suprachiasmatic nucleus (SCN) in the hypothalamus and this review summarises our current understanding of how the SCN is responsible. The oldest explanation is that cardiac circadian rhythms are the result of an acute post-translational regulation of cardiac ion channels by the autonomic nervous system under the control of the SCN – this may be involved, but current evidence is controvertible. There is good evidence that rhythms in the transcription of cardiac ion channels are involved - driven by local circadian clocks in the heart and circadian rhythms in plasma catecholamines and glucocorticoid (all ultimately under the control of the SCN). There is also a plausible suggestion that the core body temperature under the control of the SCN is involved. Understanding the processes involved will potentially highlight new ways of treating cardiac arrhythmias – for example, recently, a glucocorticoid receptor blocker has been shown to prevent the morning increase in ventricular arrhythmia susceptibility in the mouse.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"208 ","pages":"Pages 85-101"},"PeriodicalIF":4.7,"publicationDate":"2025-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145058555","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 “Human embryonic stem cell-derived cardiovascular progenitor cells stimulate cardiomyocyte cell cycle activity via activating the PI3K/Akt pathway” [J. Mol. Cell. Cardiol. 197 (2024) 5–10.]","authors":"Zhongyan Chen ,&nbsp;Xiujian Yu ,&nbsp;Minxia Ke ,&nbsp;Hao Li ,&nbsp;Yun Jiang ,&nbsp;Peng Zhang ,&nbsp;Jiliang Tan ,&nbsp;Nan Cao ,&nbsp;Huang-Tian Yang","doi":"10.1016/j.yjmcc.2025.08.011","DOIUrl":"10.1016/j.yjmcc.2025.08.011","url":null,"abstract":"","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"208 ","pages":"Pages 32-34"},"PeriodicalIF":4.7,"publicationDate":"2025-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145018441","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":"Klotho attenuates D-galactose-induced cardiac aging through the ROS/NLRP3/pyroptosis pathway","authors":"Sui-sui Wang ,&nbsp;Xu Zhang ,&nbsp;Ze-zhi Ke ,&nbsp;Yu-xin Zeng ,&nbsp;Xiu-yun Wen ,&nbsp;Wen-bin Liu ,&nbsp;Jie Zhao ,&nbsp;Xiao-dong Zhuang ,&nbsp;Li-zhen Liao","doi":"10.1016/j.yjmcc.2025.09.004","DOIUrl":"10.1016/j.yjmcc.2025.09.004","url":null,"abstract":"<div><h3>Objective</h3><div>Activation of NLRP3 inflammasome contributes to cardiac aging progression. Klotho, a recognised anti-aging protein, exerts protective effects against cardiac aging. In this study, we aimed to elucidate the protective effects of Klotho on D-galactose (D-gal)-induced cardiac aging and the underlying mechanisms.</div></div><div><h3>Methods</h3><div>Aging severity in mice was evaluated based on coat condition and serum Klotho levels. Serum levels of interleukin (IL)-1β,<!--> <!-->lactate dehydrogenase (LDH), superoxide dismutase (SOD), and malondialdehyde were measured to assess cardiac oxidative stress and inflammatory response damage. Cardiac function was evaluated using echocardiography, whereas heart histopathological changes were observed through haematoxylin-eosin (HE) staining, Masson staining, and heart index. Cardiac aging was further assessed with β-galactosidase staining and western blot analysis of aging-related proteins (P53 and P21). Pyroptosis-related protein expression was assessed via western blot, and cardiac tissue reactive oxygen species (ROS) expression levels were determined through dihydroethidium staining. Similar analyses were conducted on D-gal-treated H9C2 cardiomyocytes.</div></div><div><h3>Results</h3><div>Compared to wild-type aged mice, Klotho-treated and NLRP3 knockout mice showed markedly reduced back hair loss, elevated serum Klotho and SOD levels, reduced serum IL-1β and LDH, enhanced left ventricular ejection fraction, left ventricular fractional shortening, peak E to peak A ratio, diminished heart size, cardiomyocyte hypertrophy and collagen deposition. Decreased cardiac aging markers, apoptosis-associated speck-like protein (ASC) formation, NLRP3 expression, cleaved-caspase-1, gasdermin D (GSDMD), IL-1β, and IL-18, and lower ROS levels were observed in cardiac tissues. These protective effects were abolished upon Nigericin injection.</div></div><div><h3>Conclusions</h3><div>Klotho delays D-gal-induced cardiac aging by regulating the ROS/NLRP3/pyroptosis pathway.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"208 ","pages":"Pages 35-48"},"PeriodicalIF":4.7,"publicationDate":"2025-09-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145033545","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":"Flow cytometry of the myocardium: An end-to-end analysis of adult cardiomyocytes isolated from pig and mouse hearts","authors":"Alex Gallinat,&nbsp;Xisheng Li,&nbsp;Nikhil P. Raisinghani,&nbsp;Sabrina La Salvia,&nbsp;Anh Phan,&nbsp;Shihong Zhang,&nbsp;Spyros A. Mavropoulos,&nbsp;Samta Veera,&nbsp;Seonghun Yoon,&nbsp;Kiyotake Ishikawa,&nbsp;Susmita Sahoo","doi":"10.1016/j.yjmcc.2025.09.003","DOIUrl":"10.1016/j.yjmcc.2025.09.003","url":null,"abstract":"<div><div>Selective therapeutic targeting of cardiomyocytes (CMs) and non-myocytes (NMs) within the heart is an active field of research. The success of those novel therapeutic strategies is linked to the ability to accurately assess uptake and gene delivery efficiencies in clinically relevant animal models. Nevertheless, quantification at the single cell level remains a significant challenge. While flow cytometry offers the possibility of an accurate and direct single-cell quantification, the unique structural and physical properties of CMs complicate the analysis. There are no standardized methods reported for the flow cytometry analysis of adult CMs, which is a significant pitfall in the field. Here, we address this gap and introduce a robust and optimized method for the successful flow cytometry analysis of isolated CMs. Starting from tissue digestion, we present a simple workflow for the isolation and characterization of CMs and NMs, tested and validated for pig and mouse. We demonstrate the versatility of this method through three biologically relevant applications. First, we introduce a model to quantify CMs nucleation based on DNA content distribution. Second, we assess cell-specific <em>in vivo</em> gene delivery with AAV-Luc in pig hearts. And last, we demonstrate how structural remodeling of CMs affects their light scattering properties, in a pressure overload-induced hypertrophy mouse model. Together, these findings establish a flexible and quantitative platform for single-cell analysis of cardiac cell populations in both basic and translational cardiovascular research.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"208 ","pages":"Pages 49-59"},"PeriodicalIF":4.7,"publicationDate":"2025-09-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145008310","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}