Results 151 to 160 of about 145,724 (263)

The effects of sodium–glucose cotransporter 2 inhibitors on the ‘forgotten’ right ventricle

ESC Heart Failure, Volume 12, Issue 2, Page 1045-1058, April 2025.
Abstract With the progress in diagnosis, treatment and imaging techniques, there is a growing recognition that impaired right ventricular (RV) function profoundly affects the prognosis of patients with heart failure (HF), irrespective of their left ventricular ejection fraction (LVEF).
Liangzhen Qu, Xueting Duan, Han Chen
wiley   +1 more source

Advances in targeting myocardial fibrosis: integrating mechanisms and therapeutics. [PDF]

Front Cardiovasc Med
Xu Z, Zhao Y.
europepmc   +1 more source

Interventional therapies for chronic heart failure: An overview of recent developments

ESC Heart Failure, Volume 12, Issue 2, Page 1081-1094, April 2025.
Abstract Heart failure (HF), the final manifestation of most cardiovascular diseases, has become a major global health concern, affecting millions of individuals. Despite basic drug treatments, patients present with high morbidity and mortality rates. However, recent advancements in interventional therapy have shown promising results in improving the ...
Bingchen Guo, Si Shi, Yutong Guo, Jie Xiong, Bo Wang, Zengxiang Dong, Dianyu Gao, Yingfeng Tu   +7 more
wiley   +1 more source

Ranitidine attenuates myocardial fibrosis by suppressing histamine/H2 receptor signaling and FAK/Src activation. [PDF]

Front Pharmacol
Yang L, Zhang J, Zhao J, He M, Zheng Q, Chen H, Hu Y, Long P, Chen X.   +8 more
europepmc   +1 more source

Transendocardial injection of expanded autologous CD34+ cells after myocardial infarction: Design of the EXCELLENT trial

ESC Heart Failure, Volume 12, Issue 2, Page 1455-1463, April 2025.
Abstract Aims The extent of irreversible cardiomyocyte necrosis after acute myocardial infarction (AMI) is a major determinant of residual left ventricular (LV) function and clinical outcome. Cell therapy based on CD34+ cells has emerged as an option to help repair the myocardium and to improve outcomes.
Jerome Roncalli, François Roubille, Nicolas Meyer, Giulio Pompilio, Lionel Leroux, Philippe Henon, Guillaume Trebuchet, Anthony Criquet, Matthieu de Kalbermatten, Eric Saloux, Alain Manrique, Pierre‐Yves Marie, Deepak L. Bhatt, Scott D. Solomon, Gilles Montalescot, David E. Newby, Faiez Zannad, on behalf of the EXCELLENT Trial Investigators   +17 more
wiley   +1 more source

Composition and Influence of Fibrogenic Niche in Myocardial Fibrosis. [PDF]

Rev Cardiovasc Med
Wang X, Fan L, Yuan Q, Luo Y, Cheng Z, Chen Y, Gong C.   +6 more
europepmc   +1 more source

Circulating Endotrophin Predicts Myocardial Fibrosis Burden and Is Sensitive to Antifibrotic Therapy. [PDF]

JACC Adv
Black N, Lewis G, Soltani F, Dodd S, Williams SG, Schelbert EB, Laursen C, Angeli E, Reese-Petersen AL, Karsdal M, Genovese F, Miller CA.   +11 more
europepmc   +1 more source

Myocardial inflammation is associated with impaired mitochondrial oxidative capacity in ischaemic cardiomyopathy

ESC Heart Failure, Volume 12, Issue 2, Page 1246-1255, April 2025.
Abstract Aims Myocardial inflammation and impaired mitochondrial oxidative capacity are hallmarks of heart failure (HF) pathophysiology. The extent of myocardial inflammation in patients suffering from ischaemic cardiomyopathy (ICM) or dilated cardiomyopathy (DCM) and its association with mitochondrial energy metabolism are unknown.
Julius Borger, Elric Zweck, Constanze Moos, Patrick Horn, Fabian Voß, Heinz‐Peter Schultheiss, Jacob Eifer Møller, Udo Boeken, Hug Aubin, Artur Lichtenberg, Malte Kelm, Michael Roden, Amin Polzin, Ralf Westenfeld, Julia Szendroedi, Daniel Scheiber   +15 more
wiley   +1 more source

MYC promotes myocardial fibrosis via METTL1-mediated m7G modification of HILPDA. [PDF]

Biol Direct
Liu Y, Li K, Chen Y, Xia H.
europepmc   +1 more source

Metabolic abnormalities and reprogramming in cats with naturally occurring hypertrophic cardiomyopathy

ESC Heart Failure, Volume 12, Issue 2, Page 1256-1270, April 2025.
Abstract Background and aims The heart is a metabolic organ rich in mitochondria. The failing heart reprograms to utilize different energy substrates, which increase its oxygen consumption. These adaptive changes contribute to increased oxidative stress.
Qinghong Li, Max Homilius, Erin Achilles, Laura K. Massey, Victoria Convey, Åsa Ohlsson, Ingrid Ljungvall, Jens Häggström, Brittany Vester Boler, Pascal Steiner, Sharlene Day, Calum A. MacRae, Mark A. Oyama   +12 more
wiley   +1 more source