JACC: Basic to Translational Science最新文献_第2页

The Role of Tet2 in Medial Vascular Calcification Tet2在内侧血管钙化中的作用。

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-04-01 Epub Date: 2026-04-27 DOI: 10.1016/j.jacbts.2026.101533

Yixiao Zhu MS , Li Lin MS , Xiaoxia Wei PhD

引用次数: 0

Sodium Channel mRNA Binding Proteins 钠通道mRNA结合蛋白。

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-04-01 Epub Date: 2026-04-27 DOI: 10.1016/j.jacbts.2026.101546

Barry London MD, PhD

引用次数: 0

Recognizing Early Career Translational Investigators 认识早期职业翻译研究者。

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-04-01 Epub Date: 2026-04-27 DOI: 10.1016/j.jacbts.2026.101545

Matthias Nahrendorf MD, PhD (Editor-in-Chief: JACC: Basic to Translational Science)

引用次数: 0

Global Burden of Rheumatic Heart Disease (1990-2021), Attributable Risk Factors, and Future Projections 全球风湿性心脏病负担（1990-2021）、归因风险因素和未来预测

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-04-01 Epub Date: 2026-03-03 DOI: 10.1016/j.jacbts.2026.101511

Yuping Zou MS , Siyu Wei PhD , Qinduo Ren MS, Tianyu Zhou MS, Songlin Lu MS, Ruilin Li MS, Yingnan Ma PhD, Linna Yuan MS, Jiacheng Wang MS, Wei She MS, Xuying Guo PhD, Junxian Tao PhD, Shuo Bi MS, Hongsheng Tian MS, Chen Sun PhD, Haiyan Chen PhD, Jing Xu PhD, Yu Dong MS, Jingxuan Kang PhD, Hongchao Lv PhD, Mingming Zhang PhD

{"title":"Global Burden of Rheumatic Heart Disease (1990-2021), Attributable Risk Factors, and Future Projections","authors":"Yuping Zou MS , Siyu Wei PhD , Qinduo Ren MS, Tianyu Zhou MS, Songlin Lu MS, Ruilin Li MS, Yingnan Ma PhD, Linna Yuan MS, Jiacheng Wang MS, Wei She MS, Xuying Guo PhD, Junxian Tao PhD, Shuo Bi MS, Hongsheng Tian MS, Chen Sun PhD, Haiyan Chen PhD, Jing Xu PhD, Yu Dong MS, Jingxuan Kang PhD, Hongchao Lv PhD, Mingming Zhang PhD","doi":"10.1016/j.jacbts.2026.101511","DOIUrl":"10.1016/j.jacbts.2026.101511","url":null,"abstract":"<div><div>Rheumatic heart disease (RHD) is a chronic valvular disorder caused by acute rheumatic fever. It mostly affects the mitral valve and leads to thickening. The present study employs the GBD (Global Burden of Diseases, Injuries, and Risk Factors Study 2021) to analyze the global burden of RHD. The study investigates trends in incidence, prevalence, disability-adjusted life-years, and mortality from 1990 to 2021 across regions and 204 countries and territories, exploring difference with sex, age, and sociodemographic index. Two-sample Mendelian randomization identified high systolic blood pressure and high body mass index as causal risk factors for RHD. Although there was a slight increase in age-standardized prevalence and incidence rates, there was a decline in mortality and disability-adjusted life-year rates. Projections indicate a persistent upward trend in the incidence of the condition from 2022 to 2050. The findings emphasize the persistent global burden of RHD and underscore the necessity for targeted interventions.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"11 4","pages":"Article 101511"},"PeriodicalIF":8.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147355131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Rethinking Obesity Through the Lens of Lipid Spillover 从脂质溢出的角度重新思考肥胖问题。

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-04-01 Epub Date: 2026-04-27 DOI: 10.1016/j.jacbts.2026.101532

Shaun Khanna MBBS, MMed , Nitesh Nerlekar MBBS, PhD , Aditya Bhat MBBS, DrPH

{"title":"Rethinking Obesity Through the Lens of Lipid Spillover","authors":"Shaun Khanna MBBS, MMed , Nitesh Nerlekar MBBS, PhD , Aditya Bhat MBBS, DrPH","doi":"10.1016/j.jacbts.2026.101532","DOIUrl":"10.1016/j.jacbts.2026.101532","url":null,"abstract":"<div><div>Conventional models frame obesity as excess caloric intake but do not explain why cardiometabolic disease develops in only a subset of individuals. Building on Unger’s seminal lipotoxicity hypothesis and subsequent adipose expandability frameworks, the lipid spillover concept emphasizes adipose tissue dysfunction—rather than total fat mass—as the driver of disease. When subcutaneous adipose tissue reaches its safe storage capacity, adipocyte hypertrophy, inflammation, and insulin resistance increase lipolysis, raising circulating free fatty acids and promoting ectopic lipid deposition. Accumulation of fat in organs such as the liver, heart, skeletal muscle, pancreas, vasculature, and kidneys initiates organ-specific injury and systemic metabolic–vascular dysfunction that may occur independently of body mass index. Visceral, perivascular, and epicardial fat depots act as inflammatory reservoirs that exacerbate vascular disease and myocardial dysfunction. Advances in imaging and biomarker profiling now enable quantification of ectopic fat burden and activity, supporting risk stratification beyond body size alone. Therapeutic strategies that preferentially reduce ectopic fat through lifestyle intervention, pharmacotherapy, or bariatric surgery, offer targeted cardiometabolic risk reduction.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"11 4","pages":"Article 101532"},"PeriodicalIF":8.4,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147771937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Electrocardiographic Age and Clonal Hematopoiesis of Indeterminate Potential 心电图年龄与不确定电位的克隆造血

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-03-01 Epub Date: 2026-01-30 DOI: 10.1016/j.jacbts.2026.101486

Shaan Khurshid MD, MPH , Samuel Friedman PhD , Rakesh Rathod MS , Md Mesbah Uddin PhD , Mahnaz Maddah PhD , Michael C. Honigberg MD, MPP , Pradeep Natarajan MD, MMSc , Patrick T. Ellinor MD, PhD

引用次数: 0

Interleukin-18 Inhibition Aggravates Atherosclerosis in Jak2V617F Clonal Hematopoiesis 白细胞介素-18抑制加重Jak2V617F克隆造血的动脉粥样硬化

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-03-01 Epub Date: 2026-02-25 DOI: 10.1016/j.jacbts.2025.101463

Mojdeh Tavallaie , Cheng-Chieh Hsu , Brian D. Hardaway , Huijuan Dou , Trevor Fidler , Eunyoung Kim , Sandra E. Schiavone , David Ngai , Tong Xiao , Nan Wang , Marit Westerterp , Alan R. Tall

{"title":"Interleukin-18 Inhibition Aggravates Atherosclerosis in Jak2V617F Clonal Hematopoiesis","authors":"Mojdeh Tavallaie , Cheng-Chieh Hsu , Brian D. Hardaway , Huijuan Dou , Trevor Fidler , Eunyoung Kim , Sandra E. Schiavone , David Ngai , Tong Xiao , Nan Wang , Marit Westerterp , Alan R. Tall","doi":"10.1016/j.jacbts.2025.101463","DOIUrl":"10.1016/j.jacbts.2025.101463","url":null,"abstract":"<div><div>Clonal hematopoiesis (CH) driven by <em>JAK2</em><em><sup>V617F</sup></em> is known to accelerate atherosclerosis through inflammasome activation and release of interleukin (IL)-1β and -18; yet, the specific contribution of IL-18 has remained unclear. In this study, we demonstrate that antibody inhibition of IL-18 in <em>JAK2</em><em><sup>V617F</sup></em> CH mice increases plaque collagen but paradoxically promotes both early lesion growth and advanced necrotic core formation. Mechanistically, IL-18 blockade reverses absent in melanoma 2 inflammasome activation but shifts cell death toward apoptosis, and together with impaired efferocytosis, results in greater necrosis. These events are coordinated by reduced interferon gamma signaling, which enhances collagen deposition while decreasing expression of efferocytotic genes. Our findings challenge the prevailing notion that IL-18 inhibition stabilizes atherosclerotic plaques and provide new mechanistic insight into the interplay among inflammasome biology, adaptive immunity, and plaque stability.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"11 3","pages":"Article 101463"},"PeriodicalIF":8.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147289992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

CXCL10 Regulates Pressure Overload–Induced Heart Failure CXCL10调节压力过载引起的心力衰竭

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-03-01 Epub Date: 2026-03-23 DOI: 10.1016/j.jacbts.2025.101462

Fernando Souza-Neto PhD , Preston Le BS , Mobeen Abdrabbo BS , Ashab Alamgir BS , Haiguang Wang PhD , Natalia Ferreira de Araujo PhD , Jennifer L. Mikkila MS , Bruno Sanches MS , Preethy Parthiban PhD , Ryan Moon BS , Adam Herman PhD , Andrew B. Adams MD, PhD , Kurt W. Prins MD, PhD , Silvia Guatimosim PhD , Nathan Schuldt PhD , Xavier S. Revelo PhD , Jop H. van Berlo MD, PhD

{"title":"CXCL10 Regulates Pressure Overload–Induced Heart Failure","authors":"Fernando Souza-Neto PhD , Preston Le BS , Mobeen Abdrabbo BS , Ashab Alamgir BS , Haiguang Wang PhD , Natalia Ferreira de Araujo PhD , Jennifer L. Mikkila MS , Bruno Sanches MS , Preethy Parthiban PhD , Ryan Moon BS , Adam Herman PhD , Andrew B. Adams MD, PhD , Kurt W. Prins MD, PhD , Silvia Guatimosim PhD , Nathan Schuldt PhD , Xavier S. Revelo PhD , Jop H. van Berlo MD, PhD","doi":"10.1016/j.jacbts.2025.101462","DOIUrl":"10.1016/j.jacbts.2025.101462","url":null,"abstract":"<div><div>Heart failure is a syndrome where immune cells play a crucial role in its development and progression. Although the recruitment of T cells driven by C-X-C motif chemokine receptor 3 activation has been reported, the specific contribution of C-X-C motif chemokine ligand 10 (CXCL10), one of its ligands, remains unclear. Here, we investigate the role of CXCL10 in pressure overload–induced cardiac remodeling, both in the early phase of remodeling and during heart failure progression. We used the transverse aortic constriction model to induce pressure overload in mice and assessed the role of CXCL10 in cardiac remodeling. Our study shows that the genetic deletion of CXCL10 attenuates early cardiac remodeling and with more pronounced effects 6 weeks after transverse aortic constriction, as CXCL10–/– mice exhibit reduced hypertrophy and fibrosis and are protected from the development of cardiac dysfunction, which was observed in wild-type animals. Notably, CXCL10–/– mice do not show T-cell expansion and activation in the draining lymph nodes, particularly in the CD4+ T-cell subset. Using bone marrow chimeras, we show that CXCL10 from recruited macrophages accelerates pathologic cardiac remodeling. Our findings establish CXCL10 as a key mediator of heart failure, acting through immune cell recruitment and activation. These results suggest that targeting CXCL10 could provide a novel therapeutic strategy to mitigate inflammation-driven heart failure progression.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"11 3","pages":"Article 101462"},"PeriodicalIF":8.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147539336","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

HDL Regulates TGFβ-Receptor Lipid Raft Partitioning, Restoring Contractile Features of Cholesterol-Loaded Vascular Smooth Muscle Cells 高密度脂蛋白调节tgf β受体脂筏分配，恢复胆固醇负荷血管平滑肌细胞的收缩特征

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-03-01 Epub Date: 2026-02-12 DOI: 10.1016/j.jacbts.2025.101461

Prashanth Thevkar Nagesh PhD , Shruti Rawal PhD , Hitoo Nishi PhD , Tarik Zahr BS , Joseph M. Miano PhD , Mary Sorci-Thomas PhD , Hao Xu PhD , Naveed Akbar PhD , Robin P. Choudhury DM , Mark W. Feinberg MD , Ashish Misra PhD , Edward A. Fisher MD, PhD

{"title":"HDL Regulates TGFβ-Receptor Lipid Raft Partitioning, Restoring Contractile Features of Cholesterol-Loaded Vascular Smooth Muscle Cells","authors":"Prashanth Thevkar Nagesh PhD , Shruti Rawal PhD , Hitoo Nishi PhD , Tarik Zahr BS , Joseph M. Miano PhD , Mary Sorci-Thomas PhD , Hao Xu PhD , Naveed Akbar PhD , Robin P. Choudhury DM , Mark W. Feinberg MD , Ashish Misra PhD , Edward A. Fisher MD, PhD","doi":"10.1016/j.jacbts.2025.101461","DOIUrl":"10.1016/j.jacbts.2025.101461","url":null,"abstract":"<div><div>Many cells identified as macrophage-like in human and mouse atherosclerotic plaques are thought to be of vascular smooth muscle cell (VSMC) origin. We identified cholesterol-mediated down-regulation of TGFβ signaling in vitro in human (h)VSMCs by localization of TGFβ receptors in membrane lipid rafts, which was reversed by high-density lipoprotein (HDL)-mediated cholesterol efflux. This restored VSMC contractile marker (<em>Acta2</em>) and suppressed macrophage marker (CD68) expression by promoting TGFβ enhancement of <em>Mir145</em> expression. In vivo, administration of ApoA1 (which forms HDL) to atherosclerotic mice also promoted VSMC <em>Acta2</em> expression and reduced CD68 expression. Because macrophage-like VSMCs are thought to have adverse properties, our studies not only show mechanistically how cholesterol causes their transition, but also suggest that efflux-competent HDL particles may have a therapeutic role by restoring a more favorable phenotypic state of VSMCs in atherosclerotic plaques.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"11 3","pages":"Article 101461"},"PeriodicalIF":8.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146191007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mendelian Randomization Suggests a Causal Link Between Glycemic Traits and Thoracic Aortic Structures and Diseases 孟德尔随机化表明血糖特征与胸主动脉结构和疾病之间存在因果关系

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-03-01 Epub Date: 2026-03-23 DOI: 10.1016/j.jacbts.2026.101517

Nimrat Grewal MD, PhD , John Elefteriades MD, PhD

引用次数: 0