Abstract

Pulmonary arterial hypertension (PAH) is characterized by extensive pulmonary vascular remodeling and right ventricular failure. Metabolic deregulation has emerged as a key feature in PAH pathogenesis, involving alterations in glycolysis, fatty acid oxidation, glutaminolysis, and mitochondrial function. In this review, we examine the molecular mechanisms driving metabolic reprogramming in pulmonary vascular cells and the right ventricle, and discuss therapeutic strategies targeting metabolic pathways to reverse vascular remodeling and improve cardiac function in pulmonary hypertension.