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Fibroblast-Restricted Inflammasome Activation Promotes Atrial Fibrillation and Heart Failure With Diastolic Dysfunction. 成纤维细胞限制性炎性小体激活促进心房颤动和心力衰竭伴舒张功能障碍。
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-04-16 DOI: 10.1016/j.jacbts.2025.02.004
Luge Li, Cristian Coarfa, Yue Yuan, Issam Abu-Taha, Xiaolei Wang, Jia Song, Yuying Zeng, Xiaohui Chen, Amrit Koirala, Sandra L Grimm, Markus Kamler, Lisa K McClendon, Michelle Tallquist, Stanley Nattel, Dobromir Dobrev, Na Li
{"title":"Fibroblast-Restricted Inflammasome Activation Promotes Atrial Fibrillation and Heart Failure With Diastolic Dysfunction.","authors":"Luge Li, Cristian Coarfa, Yue Yuan, Issam Abu-Taha, Xiaolei Wang, Jia Song, Yuying Zeng, Xiaohui Chen, Amrit Koirala, Sandra L Grimm, Markus Kamler, Lisa K McClendon, Michelle Tallquist, Stanley Nattel, Dobromir Dobrev, Na Li","doi":"10.1016/j.jacbts.2025.02.004","DOIUrl":"10.1016/j.jacbts.2025.02.004","url":null,"abstract":"<p><p>Atrial fibrillation (AF) often coexists with heart failure, both involving inflammatory signaling and cardiac fibroblasts. To understand the role of fibroblast NLR family pyrin domain containing 3 (NLRP3) inflammasome in cardiac function, we found that NLRP3 was up-regulated in atrial fibroblasts from AF patients. Fibroblast-specific activation of NLRP3 in mice induced AF-promoting atrial myopathy and heart failure with diastolic dysfunction, accompanied by increased fibrosis, and reduced conduction velocity. Knockdown of NLRP3 prevented the AF-promoting atrial substrate and cardiomyopathy in the context of NLRP3 activation in fibroblasts. We identify the fibroblast NLRP3 inflammasome as a key pathway governing the promotion of proarrhythmic fibrosis in AF and cardiomyopathy.</p>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101244"},"PeriodicalIF":8.4,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144009601","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
Oversized Conduits Predict Stenosis in Tissue Engineered Vascular Grafts. 超大导管预测组织工程血管移植物狭窄。
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-04-16 DOI: 10.1016/j.jacbts.2025.02.008
Kevin M Blum, Mackenzie E Turner, Erica L Schwarz, Cameron A Best, John M Kelly, Andrew R Yates, Kan N Hor, Yuichi Matsuzaki, Joseph D Drews, Jason Zakko, Kejal Shah, Toshiharu Shinoka, Jay D Humphrey, Alison L Marsden, Christopher K Breuer
{"title":"Oversized Conduits Predict Stenosis in Tissue Engineered Vascular Grafts.","authors":"Kevin M Blum, Mackenzie E Turner, Erica L Schwarz, Cameron A Best, John M Kelly, Andrew R Yates, Kan N Hor, Yuichi Matsuzaki, Joseph D Drews, Jason Zakko, Kejal Shah, Toshiharu Shinoka, Jay D Humphrey, Alison L Marsden, Christopher K Breuer","doi":"10.1016/j.jacbts.2025.02.008","DOIUrl":"10.1016/j.jacbts.2025.02.008","url":null,"abstract":"<p><p>Tissue-engineered vascular grafts (TEVGs) offer promising advancements in treating congenital heart disease by enabling the creation of autologous tissue for complex cardiac repairs. Our approach involves implanting biodegradable scaffolds seeded with autologous cells that remodel into functional neovessels. To understand better the factors guiding neovessel formation, we evaluated 50 ovine thoracic TEVGs using angiography at 1 and 6 weeks postimplantation. Nondimensionalization accounted for anatomical differences between animals and identified hemodynamics and surgical sizing as potential driving factors. Regression analysis revealed that narrowing at the inflow anastomosis and graft oversizing correlated significantly with stenosis development. Computational fluid dynamics showed that these factors influenced wall shear stress and flow patterns, contributing to neovessel narrowing. Comparisons with clinical trial data from Fontan conduits supported these findings, emphasizing that matching graft size to the native inflow vessel can reduce stenosis and enhance TEVG performance.</p>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101248"},"PeriodicalIF":8.4,"publicationDate":"2025-04-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143967735","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
FNDC4 Prevents Aging-Related Cardiac Dysfunction: By Restoring AMPKα/PPARα-Dependent Mitochondrial Function. FNDC4通过恢复AMPKα/ ppar α依赖的线粒体功能来预防衰老相关的心功能障碍。
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-04-09 DOI: 10.1016/j.jacbts.2025.01.004
Xin Zhang, Wen-Sheng Dong, Kang Li, Yun-Jia Ye, Can Hu
{"title":"FNDC4 Prevents Aging-Related Cardiac Dysfunction: By Restoring AMPKα/PPARα-Dependent Mitochondrial Function.","authors":"Xin Zhang, Wen-Sheng Dong, Kang Li, Yun-Jia Ye, Can Hu","doi":"10.1016/j.jacbts.2025.01.004","DOIUrl":"https://doi.org/10.1016/j.jacbts.2025.01.004","url":null,"abstract":"<p><p>Mitochondria play critical roles in maintaining oxidative metabolism and cardiac homeostasis; however, their function is compromised in aging hearts. Fibronectin type III domain-containing 4 (FNDC4) is involved in regulating mitochondrial biogenesis, energy expenditure, and metabolic balance. The present study found that aging mice exhibited a sizable decline in cardiac and plasma FNDC4 levels, and that lower FNDC4 expression also correlated with a poor cardiac function. Cardiac-specific FNDC4 overexpression alleviated, while cardiac-specific FNDC4 knockdown facilitated aging-related cardiac remodeling and dysfunction. The unbiased transcriptome analysis and untargeted metabolomics revealed that FNDC4 activated AMP-activated protein kinase α/peroxisome proliferator-activated receptor α signaling pathway to improve mitochondrial dysfunction and lipotoxicity in aging hearts.</p>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101222"},"PeriodicalIF":8.4,"publicationDate":"2025-04-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215896","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
Evaluation of Treatment Effect of Sirolimus on Pediatric Pulmonary Vein Stenosis Using a Neonatal Rat Model. 西罗莫司对新生儿大鼠肺静脉狭窄治疗效果的评价。
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-04-02 DOI: 10.1016/j.jacbts.2025.01.010
Debao Li, Yingying Xiao, Peisen Ruan, Zunmin Wan, Yuqing Hu, Sijuan Sun, Zheng Wang, Sixie Zheng, Yi Yan, Hao Chen, Hao Zhang, Chun Shen, Qi Sun, Lincai Ye
{"title":"Evaluation of Treatment Effect of Sirolimus on Pediatric Pulmonary Vein Stenosis Using a Neonatal Rat Model.","authors":"Debao Li, Yingying Xiao, Peisen Ruan, Zunmin Wan, Yuqing Hu, Sijuan Sun, Zheng Wang, Sixie Zheng, Yi Yan, Hao Chen, Hao Zhang, Chun Shen, Qi Sun, Lincai Ye","doi":"10.1016/j.jacbts.2025.01.010","DOIUrl":"https://doi.org/10.1016/j.jacbts.2025.01.010","url":null,"abstract":"<p><p>A modified neonatal rat model of pulmonary vein stenosis (PVS) via bilateral pulmonary vein banding was introduced for the first time, providing a platform for understanding the pathophysiology of PVS and developing treatments. In addition, using this model, the mTOR inhibitor sirolimus was evaluated as a treatment for PVS and exhibited significant therapeutic effects, indicating the need for accelerated ethics approval in clinical settings where sirolimus is not yet in use.</p>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101229"},"PeriodicalIF":8.4,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144215895","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
Metabolic Adaptations and Therapies in Cardiac Hypoxia: Mechanisms and Clinical Implications/ Potential Strategies. 心脏缺氧的代谢适应和治疗：机制和临床意义/潜在策略。
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-04-02 DOI: 10.1016/j.jacbts.2024.12.008
Huili Li, Fei Xiao, Chenghui Zhou, Tao Zhu, Sheng Wang
{"title":"Metabolic Adaptations and Therapies in Cardiac Hypoxia: Mechanisms and Clinical Implications/ Potential Strategies.","authors":"Huili Li, Fei Xiao, Chenghui Zhou, Tao Zhu, Sheng Wang","doi":"10.1016/j.jacbts.2024.12.008","DOIUrl":"https://doi.org/10.1016/j.jacbts.2024.12.008","url":null,"abstract":"<p><p>Cardiac hypoxia triggers a cascade of responses and functional changes in myocardial and non-myocardial cells, profoundly affecting cellular metabolism, oxygen-sensing mechanisms, and immune responses. Myocardial cells, being the primary cell type in cardiac tissue, undergo significant alterations in energy metabolism, including glycolysis, fatty acid metabolism, ketone body utilization, and branched-chain amino acid metabolism, to maintain cardiac function under hypoxic conditions. Non-myocardial cells, such as fibroblasts, endothelial cells, and immune cells, although fewer in number, play crucial roles in regulating cardiac homeostasis, maintaining structural integrity, and responding to injury. This review discusses the metabolic reprogramming of immune cells, particularly macrophages, during ischemia-reperfusion injury and explores various therapeutic strategies that modulate these metabolic pathways to protect the heart during hypoxia. Understanding these interactions provides valuable insights and potential therapeutic targets for heart disease treatment.</p>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":""},"PeriodicalIF":8.4,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144015014","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
The Impact of Semaglutide on Cardiac Mass and Function Requires Further Investigation 西马鲁肽对心脏质量和功能的影响有待进一步研究
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-04-01 DOI: 10.1016/j.jacbts.2025.02.027
Qiang Xu MD , Yuqin Mao PhD , Xinyu Weng PhD , Li Shen MD , Junbo Ge MD
{"title":"The Impact of Semaglutide on Cardiac Mass and Function Requires Further Investigation","authors":"Qiang Xu MD ,&nbsp;Yuqin Mao PhD ,&nbsp;Xinyu Weng PhD ,&nbsp;Li Shen MD ,&nbsp;Junbo Ge MD","doi":"10.1016/j.jacbts.2025.02.027","DOIUrl":"10.1016/j.jacbts.2025.02.027","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 4","pages":"Pages 508-509"},"PeriodicalIF":8.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882528","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
Biliary Metaplasia and Macrophage Activation Define the Cellular Landscape of Cardiogenic Liver Disease 胆道化生和巨噬细胞活化决定心源性肝病的细胞景观
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-04-01 DOI: 10.1016/j.jacbts.2024.12.003
Arick C. Park MD, PhD , Christina F. Fu BS , Adeesh Parvathaneni BS , Bin Q. Yang MD , Mandy M. Chan BS , Kathleen Byrnes MD , Joel D. Schilling MD, PhD
{"title":"Biliary Metaplasia and Macrophage Activation Define the Cellular Landscape of Cardiogenic Liver Disease","authors":"Arick C. Park MD, PhD ,&nbsp;Christina F. Fu BS ,&nbsp;Adeesh Parvathaneni BS ,&nbsp;Bin Q. Yang MD ,&nbsp;Mandy M. Chan BS ,&nbsp;Kathleen Byrnes MD ,&nbsp;Joel D. Schilling MD, PhD","doi":"10.1016/j.jacbts.2024.12.003","DOIUrl":"10.1016/j.jacbts.2024.12.003","url":null,"abstract":"<div><div>Right heart failure significantly impacts liver remodeling and function, a process referred to as cardiogenic liver disease. Although recognized as a risk factor for adverse outcomes, little is understood about the cellular and molecular players that contribute to liver disease in heart failure. Using human liver biopsy samples from patients with heart failure and a mouse model of liver congestion, we unraveled a nexus of macrophages, hepatic stellate cells, and biliary metaplastic cells that shape the pathologic environment of cardiogenic liver disease.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 4","pages":"Pages 434-454"},"PeriodicalIF":8.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882417","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
Advancing Secondary Prevention Post-Myocardial Infarction With CSL112 CSL112促进心肌梗死后二级预防
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-04-01 DOI: 10.1016/j.jacbts.2025.01.015
Nathalie Pamir PhD , Rifat Eralp Ulusoy MD
{"title":"Advancing Secondary Prevention Post-Myocardial Infarction With CSL112","authors":"Nathalie Pamir PhD ,&nbsp;Rifat Eralp Ulusoy MD","doi":"10.1016/j.jacbts.2025.01.015","DOIUrl":"10.1016/j.jacbts.2025.01.015","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 4","pages":"Pages 419-421"},"PeriodicalIF":8.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882526","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
JACC: Basic to Translational Science 2024 Thomas Force Young Investigator Award Winner JACC：基础到转化科学2024年Thomas Force青年研究者奖得主
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-04-01 DOI: 10.1016/j.jacbts.2025.01.021
Douglas L. Mann MD (Editor-in-Chief: JACC: Basic to Translational Science)
{"title":"JACC: Basic to Translational Science 2024 Thomas Force Young Investigator Award Winner","authors":"Douglas L. Mann MD (Editor-in-Chief: JACC: Basic to Translational Science)","doi":"10.1016/j.jacbts.2025.01.021","DOIUrl":"10.1016/j.jacbts.2025.01.021","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 4","pages":"Pages 547-548"},"PeriodicalIF":8.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882414","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
Apolipoprotein A1 (CSL112) Increases Lecithin-Cholesterol Acyltransferase Levels in HDL Particles and Promotes Reverse Cholesterol Transport 载脂蛋白A1 （CSL112）增加高密度脂蛋白颗粒中卵磷脂-胆固醇酰基转移酶水平并促进胆固醇逆向转运
IF 8.4 1区 医学
JACC: Basic to Translational Science Pub Date : 2025-04-01 DOI: 10.1016/j.jacbts.2024.11.001
Rommel A. Mathias PhD , Elena Velkoska PhD , Svetlana A. Didichenko PhD , Brandon H. Greene PhD , Xiahui Tan PhD , Alexey V. Navdaev PhD , Heidi L. Collins PhD , Steven J. Adelman PhD , Kyal Young BSc , Andreas Gille MD, PhD , Danielle Duffy MD , C. Michael Gibson MSc, MD , Matthias Pelzing PhD , Bronwyn A. Kingwell PhD
{"title":"Apolipoprotein A1 (CSL112) Increases Lecithin-Cholesterol Acyltransferase Levels in HDL Particles and Promotes Reverse Cholesterol Transport","authors":"Rommel A. Mathias PhD ,&nbsp;Elena Velkoska PhD ,&nbsp;Svetlana A. Didichenko PhD ,&nbsp;Brandon H. Greene PhD ,&nbsp;Xiahui Tan PhD ,&nbsp;Alexey V. Navdaev PhD ,&nbsp;Heidi L. Collins PhD ,&nbsp;Steven J. Adelman PhD ,&nbsp;Kyal Young BSc ,&nbsp;Andreas Gille MD, PhD ,&nbsp;Danielle Duffy MD ,&nbsp;C. Michael Gibson MSc, MD ,&nbsp;Matthias Pelzing PhD ,&nbsp;Bronwyn A. Kingwell PhD","doi":"10.1016/j.jacbts.2024.11.001","DOIUrl":"10.1016/j.jacbts.2024.11.001","url":null,"abstract":"<div><div>Although high-density lipoprotein (HDL) cholesterol is inversely correlated with cardiovascular risk, an emerging paradigm is focused on increasing reverse cholesterol transport (RCT) and HDL function via apolipoprotein A1 (ApoA1). The objective of this study was to investigate the effect of ApoA1 (CSL112) infusion on HDL protein composition, cholesterol esterification rate (CER), and cholesterol efflux capacity (CEC) in patients treated after acute myocardial infarction. CSL112 reduced levels of apolipoproteins A2, B, C, and E and serum amyloids A1 and A4, whereas ApoA1, ApoM, and lecithin-cholesterol acyltransferase were significantly elevated. Increased CEC, plasma HDL cholesterol levels, CER, and CEC also were observed in CSL112-treated patients.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 4","pages":"Pages 405-418"},"PeriodicalIF":8.4,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143882525","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
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