Pub Date : 2025-09-01DOI: 10.1016/j.jacbts.2025.101374
Laura M. Dionisio , Jose A. Cancelas
{"title":"Freeze-Dried Platelet-Derived Hemostatic Products to Treat Bleeding in Dual Antiplatelet Therapy","authors":"Laura M. Dionisio , Jose A. Cancelas","doi":"10.1016/j.jacbts.2025.101374","DOIUrl":"10.1016/j.jacbts.2025.101374","url":null,"abstract":"","PeriodicalId":14831,"journal":{"name":"JACC: Basic to Translational Science","volume":"10 9","pages":"Article 101374"},"PeriodicalIF":8.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145117693","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}
Pub Date : 2025-09-01DOI: 10.1016/j.jacbts.2025.03.009
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
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.
{"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}
Pub Date : 2025-09-01DOI: 10.1016/j.jacbts.2025.02.013
Melanie P. Hager , Paulamy Ganguly , George V. Letsou
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.
{"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}
Pub Date : 2025-09-01DOI: 10.1016/j.jacbts.2025.101349
Bénédicte Gaborit MD, PhD
{"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}
Pub Date : 2025-09-01DOI: 10.1016/j.jacbts.2025.101373
Lewis J. Rubin MD
{"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}
Pub Date : 2025-09-01DOI: 10.1016/j.jacbts.2025.03.014
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
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.
{"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}
扫码关注我们
求助内容：
应助结果提醒方式：
京公网安备 11010802042870号