JACC: Basic to Translational Science最新文献_第8页

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

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 : 2026-03-01 Epub Date: 2026-03-23 DOI: 10.1016/j.jacbts.2026.101515

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

引用次数: 0

RIG-I–Adjuvanted Immunogen Elicited T-Cell Immunity Controls Trypanosoma cruzi, Chagasic Cardiomyopathy, and Left Ventricular Dysfunction rig - i佐剂免疫原诱导的t细胞免疫控制克氏锥虫病、恰加斯型心肌病和左心室功能障碍

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.2026.101508

Nandadeva Lokugamage PhD , Allison Wyrick BS , Subhadip Choudhuri PhD , Maher Raja BS , Imran H. Chowdhury PhD , Siddhartha De PhD , Upendra Marathi PhD , Nisha Jain Garg PhD, MBA

引用次数: 0

Nervous Control of Myocardial Infarction Outcomes 心肌梗死结果的神经控制

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.2026.101509

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

引用次数: 0

Can Vaccination Prevent the Development of Chagas Disease Cardiomyopathy? 接种疫苗能预防恰加斯病心肌病的发展吗？

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.2026.101513

Edecio Cunha-Neto MD, PhD , Daniela Santoro Rosa PhD

引用次数: 0

Abnormal Lipid Signaling Characterizes Diastolic Dysfunction in Pediatric Cardiomyopathy 异常脂质信号是小儿心肌病舒张功能障碍的特征。

IF 8.4 1区医学

JACC: Basic to Translational Science Pub Date : 2026-03-01 Epub Date: 2026-02-17 DOI: 10.1016/j.jacbts.2026.101491

Andrei L. Turinsky PhD , Nour Hanafi MHSc , Abdelrahman Said PhD , Caroline Kinnear MSc , Robert Lesurf PhD , José Luis López-Guillén MD , Rajadurai Akilen PhD , Suhani Patel MSc, MD , Guoliang Meng PhD , Wei Wei MSc , Isabelle Robillard Frayne MSc , Caroline Daneault PhD , Luc Mertens MD , James Ellis PhD , Matthieu Ruiz PhD , Seema Mital MD

{"title":"Abnormal Lipid Signaling Characterizes Diastolic Dysfunction in Pediatric Cardiomyopathy","authors":"Andrei L. Turinsky PhD , Nour Hanafi MHSc , Abdelrahman Said PhD , Caroline Kinnear MSc , Robert Lesurf PhD , José Luis López-Guillén MD , Rajadurai Akilen PhD , Suhani Patel MSc, MD , Guoliang Meng PhD , Wei Wei MSc , Isabelle Robillard Frayne MSc , Caroline Daneault PhD , Luc Mertens MD , James Ellis PhD , Matthieu Ruiz PhD , Seema Mital MD","doi":"10.1016/j.jacbts.2026.101491","DOIUrl":"10.1016/j.jacbts.2026.101491","url":null,"abstract":"<div><div>Pediatric cardiomyopathy is a major cause of diastolic heart failure; yet, its mechanisms remain unclear. Global myocardial transcriptomic and blood lipidomic profiling revealed a distinct metabolic signature of diastolic dysfunction marked by dysregulated lipid signaling. A machine learning model using these gene markers accurately classified diastolic dysfunction across cardiomyopathy subtypes. Lipidomic changes included excess saturated lipids and impaired oxidation that correlated with myocardial gene expression. Induced pluripotent stem cell cardiomyocytes from patients with diastolic dysfunction exhibited lipid accumulation, and mitochondrial dysfunction that was rescued by semaglutide. These findings define a new molecular phenotype of diastolic dysfunction and point to abnormal lipid signaling as a promising therapeutic target in childhood cardiomyopathy.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"11 3","pages":"Article 101491"},"PeriodicalIF":8.4,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146219931","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