Pulmonary hypertension (PH) is a fatal cardiovascular disorder characterized by the remodeling of pulmonary vasculature, which serves as a key pathological feature. Treatment options remain constrained, and significant gaps persist in our foundational, clinical, and translational knowledge, thereby necessitating further investigation. Extensive evidence suggests that dysfunction in diverse types of vascular cells plays a critical role in the pathogenesis of PH, with metabolic reprogramming profoundly influencing this process. Nevertheless, the precise molecular mechanisms involved remain poorly understood. Recent studies indicate that epigenetic abnormalities modulate cellular metabolism by altering the gene expression of essential metabolic enzymes, either directly or indirectly. As the role of epigenetics in PH becomes progressively elucidated, it offers promise for establishing a coherent framework for understanding metabolic reprogramming in cells affected by PH. This review concentrates on the alterations in glucose, lipid, and amino acid metabolism of vascular cells within the framework of pulmonary hypertension and delineates the advancements in research concerning epigenetic modifications linked to metabolic regulation in this condition. The reversibility of epigenetic modifications provides the opportunity to rectify their aberrant states. Consequently, targeting epigenetic modifications is considered an appealing therapeutic target for pulmonary hypertension. Finally, we provide a comprehensive summary of the prospects and challenges associated with potential therapeutic strategies for pulmonary hypertension, which are predicated on the reprogramming of vascular cell metabolism via epigenetic modifications.