Journal of molecular and cellular cardiology最新文献

{"title":"Corrigendum to “MMP19 in vascular smooth muscle cells protects against thoracic aortic aneurysm and dissection via the MMP19/Aggrecan/Wnt/β-catenin axis”[J Mol Cell Cardiol. 202 (2025) 35–49]","authors":"Baihui Ma , Qingyi Zeng , Fangfang Yang , Hang Yang , Wenke Li , Rei Fu , Zeyu Cai , Guoyan Zhu , Mingyao Luo , Zhou Zhou","doi":"10.1016/j.yjmcc.2025.08.002","DOIUrl":"10.1016/j.yjmcc.2025.08.002","url":null,"abstract":"","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"207 ","pages":"Pages 107-108"},"PeriodicalIF":4.7,"publicationDate":"2025-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957621","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":"Response to: Cytoplasmic RBM20 gain-of-function induces atrial arrhythmogenicity independent of splicing defects in a novel murine model by Brijesh Sathian et al.","authors":"Kensuke Ihara","doi":"10.1016/j.yjmcc.2025.08.006","DOIUrl":"10.1016/j.yjmcc.2025.08.006","url":null,"abstract":"","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"207 ","pages":"Pages 64-65"},"PeriodicalIF":4.7,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144889316","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":"A brief history of circadian time in the heart","authors":"Martin E. Young ,&nbsp;Vanya Khanna ,&nbsp;Mallory Metcalfe ,&nbsp;Niruththaan Rameshkumar ,&nbsp;Sarah Harington ,&nbsp;Leo H. Li ,&nbsp;Janan Shoja Doost ,&nbsp;Heinrich Taegtmeyer ,&nbsp;Tami A. Martino","doi":"10.1016/j.yjmcc.2025.08.005","DOIUrl":"10.1016/j.yjmcc.2025.08.005","url":null,"abstract":"<div><div>This review tracks the discovery of circadian biology in cardiovascular science, starting with early clinical observations of daily changes in heart rate, blood pressure, and cardiovascular events. These patterns suggested that time of day matters, but it was not until the past two decades that the mechanisms and knowledge translation of these rhythms were uncovered. We describe the heart's intrinsic circadian properties and importantly how this leads to regulation of cardiac gene and protein expression, neuroendocrine and vascular rhythms, metabolism, cellular electrophysiology, and cell signaling pathways. Next, we explore emerging themes, including the impact of circadian timing on ischemic injury, cardiac aging, and trends in circadian desynchrony, sex, and interorgan crosstalk. Building on these discoveries, circadian medicine is beginning to reshape clinical care including timing of surgery, chronotherapies, biomarkers, ICU design, novel molecular drugs targeting the circadian clock, the role of the microbiome and time restricted eating, the new field of rest, and the concept of One Health and applications to veterinary medicine. Looking ahead we address new frontiers such as epigenetics, gene editing, and spaceflight. Together, these advances offer a roadmap for how circadian rhythms can be harnessed to improve cardiovascular health and disease outcomes, supporting longer and healthier lives.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"207 ","pages":"Pages 66-80"},"PeriodicalIF":4.7,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144891963","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":"Long-term exercise training is associated with unique cardiac troponin I phosphorylation pattern and benign myocardial hypertrophy in the right ventricle in an experimental model of exercise-induced myocardial remodelling","authors":"Attila Oláh ,&nbsp;Beáta Bódi ,&nbsp;Bálint András Barta ,&nbsp;Olívia Bottlik ,&nbsp;Alex Ali Sayour ,&nbsp;Mihály Ruppert ,&nbsp;Karolina Katarzyna Kolodziejska ,&nbsp;Andrea Kovács ,&nbsp;Zoltán V. Varga ,&nbsp;Péter Ferdinandy ,&nbsp;Oliver Schilling ,&nbsp;Zoltán Papp ,&nbsp;Béla Merkely ,&nbsp;Tamás Radovits","doi":"10.1016/j.yjmcc.2025.08.008","DOIUrl":"10.1016/j.yjmcc.2025.08.008","url":null,"abstract":"<div><h3>Background</h3><div>Research projects have focused on exercise-induced alterations of the right ventricle (RV) of the heart, because the exercise-associated disproportionate load on the RV might lead to pathological consequences, such as interstitial fibrosis, chamber dilation or pro-arrhytmic remodelling. We aimed at providing a complex characterization of RV alterations induced by regular training in a rat model of exercise-induced cardiac remodelling.</div></div><div><h3>Methods</h3><div>Young, adult rats were divided into control (Co) and exercised (Ex) groups. Exercised rats swam 200 min/day for 12 weeks. In vivo cardiac electrophysiological study and in vitro force measurements on isolated permeabilized RV cardiomyocytes were performed to investigate electrical and functional alterations, respectively. Molecular biological and histological investigations were carried out.</div></div><div><h3>Results</h3><div>Exercise training was associated with mild increased RV hypertrophy (cardiomyocyte diameter: 12.5 ± 0.1 μm Co vs. 13.7 ± 0.2 μm Ex, <em>p</em> &lt; 0.05) and corresponding hyperphosphorylation of protein kinase B (Akt). Absence of pathological remodelling was revealed by unchanged pro-fibrotic and pro-apoptotic markers. We found increased maximal force development (12.1 ± 1.0kN/m² Co vs. 16.7 ± 1.1 kN/m² Ex, <em>p</em> &lt; 0.05) and improved calcium sensitivity in the cardiomyocytes of exercised animals. Sarcomere protein investigations revealed marked overall and site-specific (Ser22/23, Ser43 and Thr143) hypophosphorylation of troponinI. We found prolonged QT interval (repolarization) and RV effective refracter period along with decreased gene expression of potassium channels. We could not induce any ventricular arrhythmia by programmed stimulation.</div></div><div><h3>Conclusions</h3><div>Regular swim training induced physiological RV hypertrophy that was associated with functional improvement related to unique hypophosphorilation pattern of troponin I. A balanced exercise program without excessive exercise sessions might not be associated with induction of pathological alterations.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"207 ","pages":"Pages 81-91"},"PeriodicalIF":4.7,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144892222","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":"Paracrine IGFBP3 spatially coordinates IGF signaling to induce myocardial regeneration in mice","authors":"Shah R. Ali ,&nbsp;Ngoc Uyen Nhi Nguyen ,&nbsp;Waleed Elhelaly ,&nbsp;Ching-Cheng Hsu ,&nbsp;Shujuan Li ,&nbsp;Ivan Menendez-Montes ,&nbsp;Zhaoning Wang ,&nbsp;Miao Cui ,&nbsp;Abdallah Elnwasany ,&nbsp;Feng Xiao ,&nbsp;Jisheng Sun ,&nbsp;Suwannee Thet ,&nbsp;Nicholas T. Lam ,&nbsp;Alisson Cardoso ,&nbsp;Ana Helena Pereira ,&nbsp;Jinhu Wang ,&nbsp;Eric N. Olson ,&nbsp;Michael T. Kinter ,&nbsp;Luke I. Szweda ,&nbsp;John Shelton ,&nbsp;Hesham A. Sadek","doi":"10.1016/j.yjmcc.2025.08.004","DOIUrl":"10.1016/j.yjmcc.2025.08.004","url":null,"abstract":"<div><div>We hypothesized that the microenvironment of the regenerating neonatal mouse heart contains pro-mitotic factors. To identify non-cell-autonomous effectors of cardiomyocyte mitosis, we analyzed a transcriptomic screen of regenerating and non-regenerating hearts for differentially expressed secreted proteins. We identified IGFBP3 in this screen as a neonatal injury-associated secreted protein. IGFBP3 belongs to a family of proteins that can stabilize and sequester IGF growth factors, as well as exert IGF-independent functions. In the neonatal heart, IGFBP3 is expressed and secreted predominantly by endothelial cells following injury, notably in the border zone of the infarct. We generated loss-of-function and gain-of-function mouse models to dissect the role of IGFBP3 in myocardial regeneration. Global deletion of Igfbp3 blunted neonatal regeneration, while gain-of-function experiments using recombinant IGFBP3 or a tissue-specific ectopic Igfbp3 mouse model uncovered a pro-mitotic effect of IGFBP3 on cardiomyocytes in vitro and in the murine heart. The temporal and spatial expression of an IGFBP3 protease (PAPPA2) and IGFBP3 in the infarct zone suggests that IGFBP3 proteolysis is coordinated to locally release IGF2, which can activate an Insulin/IGF-based growth pathway to stimulate cardiomyocyte division. Collectively, our work illuminates an endothelial-cardiomyocyte crosstalk involving IGFBP3 that can mediate myocardial regeneration in the neonatal heart.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"207 ","pages":"Pages 93-106"},"PeriodicalIF":4.7,"publicationDate":"2025-08-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144883037","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":"Cell type specificity of Hippo-YAP signaling in cardiac development and disease","authors":"Jin Guan,&nbsp;Dominic P. Del Re","doi":"10.1016/j.yjmcc.2025.08.003","DOIUrl":"10.1016/j.yjmcc.2025.08.003","url":null,"abstract":"<div><div>The Hippo-YAP pathway is an evolutionarily conserved signaling module that regulates cell survival, proliferation, and differentiation to control organ size. Recent work has demonstrated critical roles for Hippo-YAP signaling in cardiac development and disease, including its ability to modulate both pathological and regenerative responses in the heart. Therefore, targeting the Hippo-YAP pathway for therapeutic benefit has gained attention and holds substantial promise for improving outcomes in patients with heart disease. Importantly, however, much of our understanding of cardiac Hippo-YAP signaling is based on studies in cardiomyocytes, and far less is known in other cell types in the heart. This review will focus primarily on the role of Hippo-YAP signaling in cardiomyocytes, cardiac fibroblasts, and macrophages, and explore how cell type-specific functions can impact heart development, as well as injury responses that can drive divergent outcomes in heart disease.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"207 ","pages":"Pages 51-63"},"PeriodicalIF":4.7,"publicationDate":"2025-08-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144867527","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":"Genetical TRPV4 deletion-associated gut microbiota alleviates cardiac dysfunction in mice with diabetic cardiomyopathy","authors":"Yanyan Zhou ,&nbsp;Teng Yang ,&nbsp;Suyang Zheng ,&nbsp;Tiantian Gan ,&nbsp;Fan Yu ,&nbsp;Guizhu Liu ,&nbsp;Tingting Zhou","doi":"10.1016/j.yjmcc.2025.08.001","DOIUrl":"10.1016/j.yjmcc.2025.08.001","url":null,"abstract":"<div><div>Diabetic cardiomyopathy (DCM) is a serious complication associated with diabetes that characterized by the cardiac dysfunction and myocardial fibrosis. Recent studies emphasize the significance of the gut-heart axis in the development of DCM. This current study investigates the effect of systematic-genetical TRPV4 knockout on DCM progression and explores the underlying mechanisms involving gut microbiota modulation and intestinal barrier integrity. The removal of TRPV4 in mice with DCM markedly enhances cardiac performance, decreases myocardial fibrosis, and modifies the composition of gut microbiota, resulting in a significant rise in <em>Bacteroides acidifaciens</em> (BA). TRPV4 deletion also upregulates tight junction proteins (Zonula occludens-1 (ZO-1), Occludin, and Claudin-1) and reduces serum lipopolysaccharide levels. Furthermore, fecal microbiota transplantation from the DCM donors with TRPV4 knockout to the DCM receptors replicates these cardioprotective effects in mice, and administration of BA improves cardiac function and relieves the fibrosis. Our study suggests that the cardioprotective effects of the genetic deletion of TRPV4 are related to changes in the gut microbiome, highlighting the importance of the connection between TRPV4, the gut, and the heart in the disease mechanism and potential therapeutic strategies for DCM.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"207 ","pages":"Pages 37-50"},"PeriodicalIF":4.7,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144821605","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":"FMO2 expression confers cardioprotection in doxorubicin therapy while preserving antitumor activity","authors":"Shuyuan Sheng ,&nbsp;Xianpeng Wu ,&nbsp;Changchen Xiao ,&nbsp;Jiamin Li ,&nbsp;Changle Ke ,&nbsp;Xinyang Hu ,&nbsp;Cheng Ni","doi":"10.1016/j.yjmcc.2025.07.018","DOIUrl":"10.1016/j.yjmcc.2025.07.018","url":null,"abstract":"<div><h3>Background</h3><div>Doxorubicin (DOX) is a widely used anthracycline chemotherapeutic agent, but its clinical application is limited by severe side effects, particularly DOX-induced cardiomyopathy (DIC) which is closely associated with oxidative stress, DNA damage and, subsequent apoptosis. Flavin-containing monooxygenase 2 (FMO2), a cardiac-enriched enzyme, catalyzes NADPH-dependent oxidative metabolism of diverse pharmaceuticals. Our previous work demonstrated that FMO2 expression confers cardioprotective effects against ischemic cardiomyopathy; however, the role of FMO2 in DIC has not been demonstrated.</div></div><div><h3>Methods</h3><div>DIC was induced in wild-type, FMO2^−/−, and cardiomyocyte-specific FMO2-overexpressing mice. Neonatal rat ventricular myocytes were assessed following adenoviral-mediated FMO2 knockdown or overexpression. Transcriptome profiling and chromatin analysis elucidated the mechanism involving FMO2-mediated attenuation of DOX-induced DNA damage. A xenograft model was used to evaluate the impact of FMO2 on DOX's antitumor efficacy.</div></div><div><h3>Results</h3><div>FMO2 expression was suppressed in heart following DIC. Genetic ablation of FMO2 exacerbated DIC, whereas cardiomyocyte-specific FMO2 overexpression mitigated DOX-induced cardiac injury. Mechanistically, FMO2 reduced DOX-induced DNA damage by stabilizing chromatin-associated X-ray repair cross-complementing protein 4-like factor (XLF), thereby promoting DNA repair. Furthermore, FMO2 expression did not compromise DOX's antitumor efficacy.</div></div><div><h3>Conclusions</h3><div>FMO2 expression confers cardiac protection against DIC by stabilizing chromatin-associated XLF to facilitate DNA repair. Critically, cardiac FMO2 expression preserves DOX's antitumor efficacy, establishing it as a potential target for DIC management.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"207 ","pages":"Pages 1-12"},"PeriodicalIF":4.7,"publicationDate":"2025-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144767043","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":"Cardiomyocyte Janus kinase 1 (JAK1) signaling is required for cardiac homeostasis and cytokine-dependent activation of STAT3","authors":"Arasakumar Subramani ,&nbsp;Kobina Essandoh ,&nbsp;Michael Y. Young ,&nbsp;Francesca H. Marino ,&nbsp;James P. Teuber ,&nbsp;Kay-Uwe Wagner ,&nbsp;Matthew J. Brody","doi":"10.1016/j.yjmcc.2025.07.017","DOIUrl":"10.1016/j.yjmcc.2025.07.017","url":null,"abstract":"<div><div>Despite the essential role of inflammation in the pathogenesis of heart failure and other chronic cardiovascular diseases, how cardiomyocytes sense and respond to the inflammatory milieu is not well understood. Cytokine receptors respond to circulating glycoprotein 130 (gp130) family cytokines, such as interleukin-6 (IL-6) and oncostatin M (OSM), by signaling through Janus kinases (JAK) to ultimately elicit phosphorylation-dependent nuclear translocation and transcriptional activity of signal transducer and activator of transcription (STAT) proteins. JAK1 is particularly important for STAT3-dependent cytokine production and macrophage recruitment by cardiomyocytes and STAT3 promotes cardiac hypertrophy and remodeling in response to pressure overload or angiotensin-II but is protective during ischemic injury. However, the roles of JAK1 signaling in cardiac homeostasis and cardiomyocyte cytokine sensing and responsivity remain unclear. To assess the functions of JAK1 in cardiac physiology, we generated mice with cardiomyocyte-specific deletion of JAK1 and evaluated cardiac structure and function, myocardial remodeling, and intracellular signal transduction. Loss of JAK1 in cardiomyocytes results in dilated cardiomyopathy by 6 months of age, indicating cytokine receptor signaling through JAK1 is essential for cardiac physiology. Cardiomyopathy in aged mice lacking cardiomyocyte JAK1 was characterized by substantial myocardial fibrosis. Transcriptomics and gene expression analyses identified JAK1-dependent cytokine-inducible target genes in adult cardiomyocytes as putative effectors of JAK1-STAT3 in the cardiac stress response. JAK1-deficient adult cardiomyocytes were resistant to phosphorylation and nuclear translocation of STAT3 and transcriptional reprogramming in response to OSM. Collectively these data indicate cardiomyocyte JAK1 kinase activity is required for proper cardiac maturation and homeostasis and is indispensable for STAT3 activation and transcriptional responses to OSM.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"207 ","pages":"Pages 13-23"},"PeriodicalIF":4.7,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760276","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":"Identification of sus-PSMB7_0001 as a potential pro-angiogenic circular RNA in neonatal pig hearts","authors":"Haiwang Shi ,&nbsp;Pengsheng Li ,&nbsp;Hannah Prachyl,&nbsp;Rebecca Thomas,&nbsp;Ling Tang,&nbsp;Wuqiang Zhu","doi":"10.1016/j.yjmcc.2025.07.016","DOIUrl":"10.1016/j.yjmcc.2025.07.016","url":null,"abstract":"<div><div>While circular RNAs (circRNAs) regulating angiogenesis have been identified in fish and rodent hearts, their expression profiles in pig hearts remain largely unknown. This study aims to identify circRNAs that regulate angiogenesis in postnatal pig hearts. Total RNA sequencing data on pig heart tissues collected on postnatal days 1 (P1), 3 (P3), 7 (P7) and 28 (P28) were previously reported. This study analyzed conserved circRNAs associated with angiogenesis in the database. Functional studies were conducted in human umbilical vein endothelial cells (HUVECs) and hiPSC-derived endothelial cells (hiPSC-ECs). siRNA-mediated knockdown of circRNAs and miRNAs was performed to validate their functions in regulating angiogenesis. Fluorescence in situ hybridization was used to examine circRNA localization. Sus-PSMB7_0001 expression increased in pig hearts at P7 and P28 compared to P1 and P3. Knockdown of hsa-PSMB7_0025 (the human orthologue of sus-PSMB7_0001) impaired DNA synthesis, mitosis, migration, and tube formation in HUVECs and hiPSC-ECs. hsa-PSMB7_0025 negatively regulated hsa-miR-490-3p. Activation of hsa-miR-490-3p inhibited hiPSC-EC proliferation, while its inhibition promoted proliferation. Inhibition of miR-490-3p upregulated hsa-PSMB7_0025. miR-490-3p regulates five downstream effectors (TP53BP1, TMOD3, CDYL2, FOXO1, and TGFBR1) involved in cell cycle and vascular function. These findings suggest circRNA sus-PSMB7_0001 is a potential pro-angiogenic molecule in neonatal pig hearts.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"207 ","pages":"Pages 24-36"},"PeriodicalIF":4.7,"publicationDate":"2025-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144760277","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}