Rumeysa Basdas MSc , José Manuel Martínez-Cereijo MD, PhD , Ángel L. Fernández MD, PhD , Laura Reija MD , Alba Cabaleiro MSc , Susana Belén Bravo PhD , José R. González-Juanatey MD, PhD , Sonia Eiras PhD
{"title":"Semaglutide Modulates Proinflammatory Epicardial Adipogenesis With Paracrine Effects on hiPSC-Atrial Cardiomyocytes","authors":"Rumeysa Basdas MSc , José Manuel Martínez-Cereijo MD, PhD , Ángel L. Fernández MD, PhD , Laura Reija MD , Alba Cabaleiro MSc , Susana Belén Bravo PhD , José R. González-Juanatey MD, PhD , Sonia Eiras PhD","doi":"10.1016/j.jacbts.2025.03.009","DOIUrl":"10.1016/j.jacbts.2025.03.009","url":null,"abstract":"<div><div>Inflamed epicardial fat (EAT) accumulation around the myocardium and coronaries is a risk factor for cardiovascular disease. Glucagon-like peptide receptor-agonists 1 improves the insulin response and reduces EAT thickness. We aimed to demonstrate the effect of semaglutide on proinflammatory epicardial adipogenesis with paracrine effects on cardiomyocytes. Biopsies or isolated stromal cells from subcutaneous adipose tissue and EAT of 67 patients undergoing open-heart surgery were studied by real-time quantitative polymerase chain reaction, proteomics, and metabolic assays. Adipogenesis assay and paracrine effect over atrial cardiomyocytes determined that semaglutide treatment modulates proinflammatory adiposity markers FABP4 and sPLA2 in epicardial adipogenesis with a paracrine effect in atrial cardiomyocytes.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 9","pages":"Article 101277"},"PeriodicalIF":8.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144234153","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}
Melanie P. Hager , Paulamy Ganguly , George V. Letsou
{"title":"The Past, Present, and Promising Future of Direct Cardiac Compression Devices","authors":"Melanie P. Hager , Paulamy Ganguly , George V. Letsou","doi":"10.1016/j.jacbts.2025.02.013","DOIUrl":"10.1016/j.jacbts.2025.02.013","url":null,"abstract":"<div><div>Direct cardiac compression (DCC) devices, under development as a new modality for mechanical cardiac support (MCS), offer several advantages over presently available forms of MCS. DCC devices avoid the blood contact obligatory with other implantable MCS devices, the complications associated with blood contact and hematologic incompatibility, such as thrombosis, stroke, and the need for anticoagulation are avoided, and DCC does not require vascular access eliminating challenges such as bleeding and extremity ischemia. Arterial pressure pulsatility is also maintained with DCC. Significant and underappreciated advancements in DCC technology have occurred over the last decades with notable dramatic improvements in cardiac performance and minimal tissue damage. One device has entered clinical trials with a second device anticipated to follow. DCC is poorly understood by most cardiologists and cardiac surgeons. This review summarizes DCC development and advances so that upcoming human clinical trials can be properly assessed.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 9","pages":"Article 101254"},"PeriodicalIF":8.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753423","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":"Effect of Semaglutide on Epicardial Adipogenesis and hiPSC-Atrial Cardiomyocytes New Hope in Targeting Epicardial Adipose Tissue","authors":"Bénédicte Gaborit MD, PhD","doi":"10.1016/j.jacbts.2025.101349","DOIUrl":"10.1016/j.jacbts.2025.101349","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 9","pages":"Article 101349"},"PeriodicalIF":8.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117569","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":"A Gut Feeling","authors":"Lewis J. Rubin MD","doi":"10.1016/j.jacbts.2025.101373","DOIUrl":"10.1016/j.jacbts.2025.101373","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 9","pages":"Article 101373"},"PeriodicalIF":8.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117573","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}
Daniel Diaz-Gil MD , Gregor Gierlinger MD , Natalia Silva-Gomez Cand Med , Lavinia Rech MD, PhD , Jesus Ortiz-Urbina MD , Kerstin Saraci Cand Med , Sophia Koutsogiannaki PhD , Cordula M. Wolf MD , Rainer G. Kozlik-Feldmann MD , Rudolf Mair MD , Juan M. Melero-Martin PhD , Sitaram M. Emani MD , Guillermo García-Cardeña PhD , Pedro J. del Nido MD , Ingeborg Friehs MD
{"title":"Preclinical Assessment of Atorvastatin for Treatment of Endocardial Fibroelastosis","authors":"Daniel Diaz-Gil MD , Gregor Gierlinger MD , Natalia Silva-Gomez Cand Med , Lavinia Rech MD, PhD , Jesus Ortiz-Urbina MD , Kerstin Saraci Cand Med , Sophia Koutsogiannaki PhD , Cordula M. Wolf MD , Rainer G. Kozlik-Feldmann MD , Rudolf Mair MD , Juan M. Melero-Martin PhD , Sitaram M. Emani MD , Guillermo García-Cardeña PhD , Pedro J. del Nido MD , Ingeborg Friehs MD","doi":"10.1016/j.jacbts.2025.03.014","DOIUrl":"10.1016/j.jacbts.2025.03.014","url":null,"abstract":"<div><div>Endocardial fibroelastosis is a condition caused by the fibrogenic activation of endothelial cells via endothelial-to-mesenchymal transition of the endocardium, which is regulated by the transforming growth factor-β pathway. Atorvastatin, a statin, can protect the vascular endothelium by up-regulating KLF2 and inhibiting the transforming growth factor-β pathway. This study aimed to investigate the effects of atorvastatin on the fibrogenic activation of endothelial cells in the endocardium. The study found that atorvastatin treatment reduced fibrogenic activation of endocardial endothelial cells and increased KLF2 expression in both in vitro and in vivo models of endocardial fibroelastosis–related left ventricular restriction.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 9","pages":"Article 101282"},"PeriodicalIF":8.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144753422","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":"T Cells, Triglycerides, and the Immune Roots of Residual Cardiovascular Risk","authors":"Michael D. Shapiro DO, MCR","doi":"10.1016/j.jacbts.2025.101376","DOIUrl":"10.1016/j.jacbts.2025.101376","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 9","pages":"Article 101376"},"PeriodicalIF":8.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117572","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}
Nathalie A. Reilly PhD , Janneke W.C.M. Mulder MD , Koen F. Dekkers PhD , Thomas B. Kuipers BSc , Leonie C. van Vark-van der Zee BSc , Monique T. Mulder PhD , Jeanine E. Roeters van Lennep MD, PhD , J. Wouter Jukema MD, PhD , Bastiaan T. Heijmans PhD
{"title":"Triglycerides and T Cells in Cardiovascular Risk","authors":"Nathalie A. Reilly PhD , Janneke W.C.M. Mulder MD , Koen F. Dekkers PhD , Thomas B. Kuipers BSc , Leonie C. van Vark-van der Zee BSc , Monique T. Mulder PhD , Jeanine E. Roeters van Lennep MD, PhD , J. Wouter Jukema MD, PhD , Bastiaan T. Heijmans PhD","doi":"10.1016/j.jacbts.2025.101359","DOIUrl":"10.1016/j.jacbts.2025.101359","url":null,"abstract":"<div><div>Triglycerides and T cells play a key role in atherosclerosis, the leading cause of cardiovascular disease (CVD). Moderately elevated triglycerides have emerged as a causal risk factor, and T cells are a prominent component of atherosclerotic plaques. This cross-sectional study examined transcriptomic differences in T cells among patients with varying triglyceride levels via RNA sequencing. We analyzed CD4<sup>+</sup> and CD8<sup>+</sup> T cells from 49 participants, including those with primary (genetic) and secondary moderate hypertriglyceridemia, severe hypertriglyceridemia, and hypotriglyceridemia. Patients with primary moderate hypertriglyceridemia exhibited a proinflammatory transcriptomic profile, including increased interleukin-6 receptor (<em>IL6R</em>) expression, which is implicated in CVD risk. Similar patterns appeared in CD8<sup>+</sup> T cells and, to a lesser extent, in secondary moderate hypertriglyceridemia patients. Conversely, transcriptomic differences were reversed in hypotriglyceridemia and absent in severe hypertriglyceridemia patients. These findings suggest that elevated triglycerides may contribute to CVD by promoting a proinflammatory transcriptomic profile in T cells.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 9","pages":"Article 101359"},"PeriodicalIF":8.4,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144886152","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}
Alex M. Parker MBiomedSc , Jarmon G. Lees PhD , Andrew J. Murray PhD , Anida Velagic PhD , Shiang Y. Lim MPharm, PhD , Miles J. De Blasio PhD , Rebecca H. Ritchie PhD
{"title":"Precision Medicine","authors":"Alex M. Parker MBiomedSc , Jarmon G. Lees PhD , Andrew J. Murray PhD , Anida Velagic PhD , Shiang Y. Lim MPharm, PhD , Miles J. De Blasio PhD , Rebecca H. Ritchie PhD","doi":"10.1016/j.jacbts.2025.101345","DOIUrl":"10.1016/j.jacbts.2025.101345","url":null,"abstract":"<div><div>A substantial component of the increasing global burden of cardiovascular disease is attributed to heart failure (HF), affecting over 64 million adults worldwide. Maladaptive mitochondrial respiratory alterations and oxidative stress are major contributors to HF development and progression, with subsequent downstream myocardial energetic impairment as a strong predictor of mortality. Current conventional therapeutic approaches, including renin-angiotensin-aldosterone system inhibition and β-adrenergic blockade, target neurohormonal aspects of HF and are effective in slowing disease progression. However, although these therapies may be associated with some improvement in myocardial energetics, they do not specifically address alterations in myocardial mitochondrial respiration or redox homeostasis. Targeting mitochondria has hence become a promising approach for more effective and tailored therapies. This review summarizes metabolic derangements that drive HF progression, with a specific focus on mitochondria. Importantly, here we address the essential knowledge gaps in the field, highlighting key translational strategies used to date, and the challenges associated with therapeutically targeting mitochondrial pathways, alongside recent developments seeking to deploy novel mitochondrial-targeted therapeutic approaches to treat HF.</div></div>","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 9","pages":"Article 101345"},"PeriodicalIF":8.4,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144880129","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}