Abstract
Pulmonary hypertension (PH) is a progressive lethal disease, which is characterized by abnormal vascular remodeling and persistently elevated pulmonary artery pressure, eventually leading to right heart failure and even death. Although great progress has been made in treating PH, the mortality rate remains high. Metabolic disorders are one of the important hallmarks of PH. Obesity, lipids, glucose tolerance and insulin resistance are risk factors for numerous cardiovascular diseases and are often accompanied by a considerable increase in serum uric acid (SUA) concentrations. Uric acid (UA) is the end product of purine nucleotide metabolism and is closely related to cardiovascular diseases including PH. Hyperuricemia promotes the development and progression of PH through endothelial dysfunction, oxidative stress, inflammatory responses and activation of the renin‑angiotensin system. In the present review, the advancements in knowledge about UA metabolism and PH, and the current understanding of the potential interactions and mechanisms of SUA in PH were systematically summarized, which may provide new insights into the pathogenesis of PH.