Results 211 to 220 of about 218,133 (348)

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

open access: yesESC 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   +17 more
wiley   +1 more source

HIV-Associated Proteomic Signature of Myocardial Fibrosis and Incident Heart Failure. [PDF]

open access: yesJ Infect Dis
Peterson TE   +19 more
europepmc   +1 more source

AP39 Through AMPK-ULK1-FUNDC1 Pathway Regulates Mitophagy Inhibits Pyroptosis Improves Doxorubicin-Induced Myocardial Fibrosis

open access: green, 2023
Junxiong Zhao   +8 more
openalex   +1 more source

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

open access: yesESC 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   +15 more
wiley   +1 more source

Inhibiting the Histone Demethylase Kdm4a Restrains Cardiac Fibrosis After Myocardial Infarction by Promoting Autophagy in Premature Senescent Fibroblasts [PDF]

open access: gold
Ming Jin   +15 more
openalex   +1 more source

Metabolic abnormalities and reprogramming in cats with naturally occurring hypertrophic cardiomyopathy

open access: yesESC 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   +12 more
wiley   +1 more source

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