Zhuofan Li BS , Ze Gong PhD , Weihao Li MD , Yanghui Chen PhD , Rongbo Dai PhD , Shiyu Yang BS , Yufei Chen PhD , Fang Yu MS , Yi Fu MBBS, PhD , Wei Li MD , Dao Wen Wang MD, PhD , Yiting Jia PhD , Wei Kong MD, PhD
{"title":"The Reduction of COMP Serves as a Predictor for Warning of Aortic Dissection Progression","authors":"Zhuofan Li BS , Ze Gong PhD , Weihao Li MD , Yanghui Chen PhD , Rongbo Dai PhD , Shiyu Yang BS , Yufei Chen PhD , Fang Yu MS , Yi Fu MBBS, PhD , Wei Li MD , Dao Wen Wang MD, PhD , Yiting Jia PhD , Wei Kong MD, PhD","doi":"10.1016/j.jacbts.2025.101329","DOIUrl":"10.1016/j.jacbts.2025.101329","url":null,"abstract":"<div><div>Thoracic aortic dissection (TAD) is a life-threatening cardiovascular disease that is associated with high morbidity and mortality. The prevailing challenge in TAD monitoring and diagnosis is the lack of novel biomarkers. A significant and sustained reduction in plasma cartilage oligomeric matrix protein (COMP) levels was observed through a case control analysis conducted in 362 TAD patients and 136 controls. The protective role of COMP was assessed in two TAD mouse models. These data suggested that a decreased plasma COMP level might serve as a novel biomarker for TAD progression and COMP could suppress the development of TAD and ameliorate vascular pathogenesis.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101329"},"PeriodicalIF":8.4,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144655006","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}
Azariyas A. Challa MD, PhD , Bradford G. Hill PhD , Matthew A. Nystoriak PhD , Kara R. Gouwens BS , Dinesh K. Kalra MD
{"title":"Ketone Bodies in Cardiovascular Disease","authors":"Azariyas A. Challa MD, PhD , Bradford G. Hill PhD , Matthew A. Nystoriak PhD , Kara R. Gouwens BS , Dinesh K. Kalra MD","doi":"10.1016/j.jacbts.2025.101328","DOIUrl":"10.1016/j.jacbts.2025.101328","url":null,"abstract":"<div><div>Evidence for the potential of ketone bodies (KBs) in the treatment of cardiovascular disease is growing rapidly. In addition to serving as sources of myocardial fuel, KBs exert an array of pleiotropic activities via multiple mechanisms. The vasculature is emerging as a key target of KBs. Recent small clinical studies have shown that the administration of exogenous KBs to patients with heart failure is associated with a marked reduction in systemic vascular resistance and improvement in myocardial function. Exogenous KBs have also been shown to increase coronary blood flow; decrease pulmonary vascular resistance; promote endothelial function and angiogenesis; increase skeletal muscle oxygenation and capillarization; and inhibit atherosclerosis, vascular calcification, and senescence. These vasculo-protective properties likely contribute to the beneficial effects of exogenous KBs observed in heart failure, pulmonary hypertension, and myocardial ischemia/infarction, and suggest potential wide applications in several other cardiovascular diseases and related conditions. In this review, we will discuss the salutary vascular effects of KBs and their cardioprotective roles.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101328"},"PeriodicalIF":8.4,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144655007","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}
Yinda Yu MSc , Shiying Lin MSc , Yueyun Pan MSc , Ning He MSc , Yanzhao Wu MD , Osman Ahmed MD, PhD , Ulf Hedin MD, PhD , Mikael C.I. Karlsson PhD , Nailin Li MD, PhD , Anton Gisterå MD, PhD
{"title":"Atheroprotective Immunity and Interleukin-10 Linked to Reduced Characteristics of Plaque Stability","authors":"Yinda Yu MSc , Shiying Lin MSc , Yueyun Pan MSc , Ning He MSc , Yanzhao Wu MD , Osman Ahmed MD, PhD , Ulf Hedin MD, PhD , Mikael C.I. Karlsson PhD , Nailin Li MD, PhD , Anton Gisterå MD, PhD","doi":"10.1016/j.jacbts.2025.101322","DOIUrl":"10.1016/j.jacbts.2025.101322","url":null,"abstract":"<div><div>Autoimmunity to low-density lipoprotein (LDL) is linked to atherosclerosis, with LDL immunization proposed as a preventive measure, but the mechanisms of atheroprotective immunity are not well understood. We investigated T-cell responses to LDL using 2 T-cell receptor transgenic mouse strains. At 52 weeks, BT1×HuBL mice showed reduced atherosclerosis, increased humoral responses against LDL, and lower plasma cholesterol. Conversely, BT3×HuBL mice had reduced atherosclerosis without changes in cholesterol, linked to increased type 1 regulatory T cells, interleukin (IL)-10 production, and decreased characteristics of plaque stability. In human plaques, IL10 mRNA negatively correlated with collagen content, and IL-10 inhibited collagen production in vitro. We conclude that atheroprotective LDL immunity elicits 2 distinct pathways: lipid-lowering immune responses and local anti-inflammatory IL-10 production. Because IL-10 is associated with decreased plaque stability and increased risk of cardiovascular events, treatments aimed at promoting IL-10 signaling over extended periods to reduce vascular inflammation should be carefully monitored.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101322"},"PeriodicalIF":8.4,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144655005","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}
{"title":"Statins for the “SMuRFLess but Inflamed”","authors":"Paul M Ridker MD, MPH","doi":"10.1016/j.jacbts.2025.101318","DOIUrl":"10.1016/j.jacbts.2025.101318","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 8","pages":"Article 101318"},"PeriodicalIF":8.4,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144642613","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}
{"title":"Inhibition of Scarb1 on Endothelial Cells Attenuates Pressure Overload-induced Heart Failure Progression.","authors":"Toshiomi Katsuki, Dai Kusumoto, Yohei Akiba, Mai Kimura, Jin Komuro, Takahiro Nakamura, Hisayuki Hashimoto, Thukaa Kouka, Kazuhisa Sugai, Yoshinori Katsumata, Masaki Miyasaka, Yutaka Suzuki, Junko Kuramoto, Yoshiaki Kubota, Keiichi Fukuda, Shinsuke Yuasa, Masaki Ieda","doi":"10.1016/j.jacbts.2025.05.003","DOIUrl":"https://doi.org/10.1016/j.jacbts.2025.05.003","url":null,"abstract":"<p><p>Inappropriate endothelial cell (EC) interactions contribute to heart failure; however, their precise mechanisms remain poorly understood. This study investigated EC-fibroblast interactions mediated by Scarb1 using single-cell RNA-sequencing analysis in a mouse heart failure model. ECs exhibited inflammatory and fibrotic gene expression, with Scarb1-mediated fibroblast-EC interactions driving disease progression. EC-specific Scarb1 knockout and systemic SCARB1 inhibition attenuated heart failure progression. In vitro and spatial omics analyses confirmed the role of SCARB1 in ECs and cell-cell interaction during heart failure progression. These findings highlight SCARB1 as a promising therapeutic target for EC-focused interventions.</p>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":" ","pages":"101308"},"PeriodicalIF":8.4,"publicationDate":"2025-07-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144794467","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}
{"title":"The Cardiohepatic Axis in Heart Failure","authors":"Arick C. Park MD, PhD , Joel D. Schilling MD, PhD","doi":"10.1016/j.jacbts.2025.05.007","DOIUrl":"10.1016/j.jacbts.2025.05.007","url":null,"abstract":"<div><div>Cardiogenic liver disease is a sequela of hepatic congestion from right heart failure that leads to hepatic dysfunction and adverse liver remodeling. Understanding the mechanisms and consequences of liver pathology in the syndrome of heart failure is an important unmet need in the care of patients with chronic heart failure. Liver congestion provokes profound responses in hepatocytes and nonparenchymal cells including endothelial cells, macrophages, and hepatic stellate cells. However, the pathways that drive liver fibrosis and dysfunction are poorly understood. Recent human and preclinical data has begun to unravel the cellular landscape and molecular pathways that define cardiogenic liver disease. This review aims to discuss our current understanding of the cardiohepatic axis in heart failure while also highlighting knowledge gaps and opportunities for future investigation.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 7","pages":"Article 101312"},"PeriodicalIF":8.4,"publicationDate":"2025-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144721929","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}