Journal of molecular and cellular cardiology最新文献

{"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":"2025-10-01","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":"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 ,&nbsp;Qingyi Zeng ,&nbsp;Fangfang Yang ,&nbsp;Hang Yang ,&nbsp;Wenke Li ,&nbsp;Rei Fu ,&nbsp;Zeyu Cai ,&nbsp;Guoyan Zhu ,&nbsp;Mingyao Luo ,&nbsp;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":"2025-10-01","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":"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":"2025-10-01","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":"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":"2025-10-01","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":"Time-restricted feeding mediated synchronization of circadian rhythms to sustain cardiovascular health","authors":"Girish C. Melkani","doi":"10.1016/j.yjmcc.2025.07.007","DOIUrl":"10.1016/j.yjmcc.2025.07.007","url":null,"abstract":"<div><div>Circadian rhythm is critical in maintaining metabolic homeostasis, including cardiac health, with disruptions often leading to adverse cardiac outcomes. Time-restricted feeding/eating (TRF/TRE) is a dietary approach that limits food intake to specific hours during an organism's active phase, daytime for diurnal animals and nighttime for nocturnal ones. This strategy has shown promise in realigning circadian rhythms and reducing the negative effects of circadian disruption on heart function. This review examines the intricate relationship between circadian rhythms and cardiac health, highlighting the molecular mechanisms governed by central and peripheral clocks. We discuss how circadian misalignment contributes to cardiovascular disease and explore how TRF/TRE can restore circadian synchronization, particularly in the context of lipid metabolism, gene expression, and other physiological processes essential for heart function. The review also examines the impact of TRF/TRE on cardiac renovation, particularly under conditions of circadian disruption associated with cardiovascular and cardiometabolic disorders. We further explore potential molecular mechanisms, including the modulation of clock genes and lipid metabolic pathways, such as diacylglycerol O-acyltransferase 2 (DGAT2), that underpin the cardioprotective effects of TRF. By consolidating findings from genetic and translational animal models and human studies, we underscore the promise of TRF/TRE in improving cardiac outcomes and propose areas for future research. The potential of TRF/TRE as a therapeutic intervention for cardiovascular disease warrants further investigation, particularly in understanding its long-term effects on cardiac health and its integration into clinical practice.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"206 ","pages":"Pages 1-10"},"PeriodicalIF":4.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144614378","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":"Matrix metalloproteinase 9 deficiency promotes endogenous cardiomyocyte proliferation","authors":"Chenying Xiang ,&nbsp;Ning Liu ,&nbsp;Shijie Sun ,&nbsp;Haorui Liu ,&nbsp;Yifan Xie ,&nbsp;Jie Feng ,&nbsp;Miaoqing Hu ,&nbsp;Yu Nie ,&nbsp;Lina Bai","doi":"10.1016/j.yjmcc.2025.07.009","DOIUrl":"10.1016/j.yjmcc.2025.07.009","url":null,"abstract":"<div><div>Matrix metalloproteinase 9 (MMP9) is known to modulate cardiac remodeling after myocardial infarction, but its role in cardiomyocyte proliferation remains unclear. Here, we showed that MMP9 deficiency enhanced neonatal cardiomyocyte proliferation and mononucleation following apical resection. Integrated transcriptomic and proteomic analyses revealed that MMP9 knockout induces a metabolic shift from oxidative phosphorylation to glycolysis in injured neonatal hearts, coinciding with upregulation of acyl-CoA thioesterase 1 (ACOT1). ACOT1 overexpression enhanced glycolysis and proliferation in primary rat cardiomyocytes, whereas 2-Deoxy-D-glucose inhibition blocked this effect. Collectively, our findings demonstrate that MMP9 deficiency drives a metabolic shift from oxidative phosphorylation to glycolysis via ACOT1 upregulation, thereby promoting cardiomyocyte proliferation.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"206 ","pages":"Pages 70-75"},"PeriodicalIF":4.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626572","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":"Diabetic cardiomyopathy: insights into pathophysiology, diagnosis and clinical management","authors":"David Chen ,&nbsp;Andrew Sindone ,&nbsp;Michael L.H. Huang ,&nbsp;Karlheinz Peter ,&nbsp;Alicia J. Jenkins","doi":"10.1016/j.yjmcc.2025.06.013","DOIUrl":"10.1016/j.yjmcc.2025.06.013","url":null,"abstract":"<div><div>Diabetes mellitus is associated with significant morbidity and premature mortality for which heart failure (HF) is a major cause. HF may be due to ischaemia, hypertension, valvular disease, uraemia, or a specific diabetic cardiomyopathy, and multiple causes may co-exist. A recent systematic review suggests that &gt;40 % of people with type 2 diabetes have diastolic dysfunction without a reduction of cardiac systolic function. In people with type 1 diabetes without known cardiovascular disease, 16 % had systolic or diastolic dysfunction. Early diabetic cardiomyopathy is asymptomatic and can progress to symptomatic HF via increasing cardiomyocyte hypertrophy and death as well as cardiac fibrosis. The 5-year mortality rate for HF is similar or worse than many common cancers. There have been significant recent advances in HF treatment including sodium-glucose co-transport 2 inhibitors (SGLT2i) and angiotensin receptor-neprilysin inhibitors (ARNi), and promising therapies such as finerenone and glucagon-like peptide-1 receptor agonists (GLP-1RA). SGLT2i, finerenone, and GLP-1RA may also have a role in HF prevention in asymptomatic diabetic cardiomyopathy. While there is currently no specific treatment for diabetic cardiomyopathy that goes beyond general HF treatment, there is promising research into innovative technologies such as gene and stem cell therapies. Also, digital technologies will likely have an increasing role in diabetic cardiomyopathy treatment. Herein we review the pathophysiology, diagnosis, and treatment of diabetic cardiomyopathy, with a focus on existing, emerging, and potentially promising novel therapies. We provide practical tables that summarise treatments at each stage as well as important practice points for commonly prescribed drugs.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"206 ","pages":"Pages 55-69"},"PeriodicalIF":4.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144584173","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":"Anti-cancer agent Olaparib ameliorates doxorubicin-induced cardiotoxicity in vitro and in vivo","authors":"Dongqing Chen ,&nbsp;Amanda J. Croft ,&nbsp;Tatt Jhong Haw ,&nbsp;Conagh Kelly ,&nbsp;Lohis Balachandran ,&nbsp;Aaron L. Sverdlov ,&nbsp;Doan T.M. Ngo","doi":"10.1016/j.yjmcc.2025.07.015","DOIUrl":"10.1016/j.yjmcc.2025.07.015","url":null,"abstract":"<div><div>Inhibition of poly (ADP-ribose) polymerase (PARP) has shown cardioprotective effects in myocardial injury, and PARP activation has been implicated in Doxorubicin-induced cardiotoxicity (DIC). Thus, PARP inhibition may be a potential preventive therapy for DIC. The present study aims to determine the cardioprotective effects of Olaparib in preventing DIC in in vitro and in vivo models. In vitro<em>:</em> Human cardiomyocytes (HCM) were treated with Doxorubicin at 1 μM (EC50) +/− 80 μM of Olaparib for 48 and 72 h, assessing cell viability (CellTiter-Glo®) and conducted gene expression analysis; Concomitant Olaparib treatment prevented Doxorubicin-induced impairment of HCM viability. Doxorubicin induced upregulation of mRNA expressions of genes involved in apoptosis: <em>CASP3</em>; DNA damage: <em>BBC3</em>; and cardiac remodeling: <em>TGF-β</em>; −all were reversed by Olaparib. In vivo<em>:</em> Female C57BL/6 mice were administered intraperitoneally either: A) vehicle of 0.9 % saline and 8 % DMSO in PBS; B) Doxorubicin at 5 mg/kg/wk. for 5 weeks; C) Olaparib at a dose of 50 mg/kg in 8 % DMSO, administered 3 times/week; D) Olaparib at 50 mg/kg, administered 3 times/week, started one week prior to commencement of Doxorubicin treatments at 5 mg/kg/week. Serial echocardiography was performed. mRNA, protein expressions and RNA sequencing were performed in the cardiac tissues; Doxorubicin induced significant LV dysfunction after 6 weeks of treatment; whereas the mice treated with Olaparib in combination with Doxorubicin showed preservation of cardiac function. Analysis of RNA-seq and Western blot data suggested that Olaparib's cardioprotective effects in DIC may involve regulating innate immune responses by lowering cGAS-STING levels, elevated by Doxorubicin. Olaparib protects HCM against DIC both in vitro and in vivo. This is mediated in part via cGAS-STING pathway.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"206 ","pages":"Pages 114-126"},"PeriodicalIF":4.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144713407","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 “Population-based computational simulations elucidate mechanisms of focal arrhythmia following stem cell injection” [Journal of Molecular and Cellular Cardiology 204 (2025) 5–16]","authors":"Chelsea E. Gibbs ,&nbsp;Patrick M. Boyle","doi":"10.1016/j.yjmcc.2025.07.004","DOIUrl":"10.1016/j.yjmcc.2025.07.004","url":null,"abstract":"","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"206 ","pages":"Page 54"},"PeriodicalIF":4.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144656497","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":"Deregulated nutrient response in ttntv cardiomyopathy can be repaired via Erk inhibition for cardioprotective effects","authors":"Feixiang Yan ,&nbsp;Weiyue Wang ,&nbsp;Maryam Moossavi ,&nbsp;Ping Zhu ,&nbsp;Noa Odell ,&nbsp;Xiaolei Xu","doi":"10.1016/j.yjmcc.2025.07.006","DOIUrl":"10.1016/j.yjmcc.2025.07.006","url":null,"abstract":"<div><h3>Background</h3><div>Truncating TITIN variants (TTNtv) are the most prevalent genetic cause of dilated cardiomyopathy (DCM); however, key pathological signaling pathways remain elusive. We recently established a zebrafish model of TTNtv DCM and developed a F0-based genome editing technology for the rapid screening of genetic modifiers.</div></div><div><h3>Methods</h3><div>We screened multiple known cardiomyopathy signaling pathways through a F0-based genetic assay using a zebrafish <em>ttntv</em> DCM model. Because ERK signaling was identified from the screen, which was also independently identified as an altered signaling pathway during a cardiac transcriptomic study of the <em>ttntv</em> DCM model, we then assessed modifying effects of differentially expressed genes (DEGs) in ERK signaling.</div></div><div><h3>Results</h3><div><em>erk1</em> and <em>mek1</em> have been identified as therapeutic modifiers for <em>ttntv</em> DCM. Consistent with their modifying effects, we observed increased levels of phosphorylated Erk1 protein in <em>ttntv</em> adult zebrafish. Mechanistically, we showed that enhanced ERK signaling results in deregulated nutrient response, as indicated by the muted response of phosphorylated ribosomal protein S6 (pS6) expression in the heart during the fasting-refeeding cycle. The inhibition of ERK signaling is sufficient to rescue deregulated nutrient response and mitigate cardiac dysfunction. Further genetic screens of DEGs in ERK signaling identified <em>ppp1r10</em>, encoding a protein phosphatase 1 (PP1) regulatory subunit that regulates Mek1/Erk1 phosphorylation, as another therapeutic modifier gene that also rescues deregulated nutrient response.</div></div><div><h3>Conclusions</h3><div>An Erk - nutrient response signaling axis is disrupted in <em>ttntv</em> cardiomyopathy, which can be repaired by the inhibition of <em>erk1, mek1</em> or <em>ppp1r10,</em> suggesting a new therapeutic avenue for <em>TTNtv</em> DCM.</div></div>","PeriodicalId":16402,"journal":{"name":"Journal of molecular and cellular cardiology","volume":"206 ","pages":"Pages 27-38"},"PeriodicalIF":4.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626571","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}