A Translational Model of MASLD-Associated HFpEF Defines Mitochondrial Dysfunction and Cardiac Plasticity During Disease Progression and Regression
This study establishes the Alms1-/- (Foz/Foz) mouse model as a robust translational platform demonstrating that mitochondrial dysfunction and fibroinflammatory remodeling drive MASLD-associated HFpEF, a condition characterized by reversible cardiac and hepatic phenotypes upon dietary intervention.