Abstract
Pulmonary hypertension (PH) is a life-threatening condition characterized by right ventricular (RV) remodeling, which is a major determinant of patient survival. The progression of right ventricular remodeling is significantly influenced by mitochondrial dysfunction, providing profound insights into vascular health and cardiovascular risk. In this review, we discuss the molecular targets, pathophysiological characteristics, and potential mechanisms underlying mitochondrial dysfunction in PH, encompassing disturbances in mitochondrial dynamics, inflammation, and dysregulation of mitochondrial energy metabolism. Finally, we review the primary therapeutic targets currently utilized to address cardiac dysfunction resulting from mitochondrial damage. Hopefully, this might inspire novel approaches to the management of cardiovascular disorders.