Hypoxanthine Promotes Pulmonary Vascular Remodeling and Adenosine Deaminase Is a Therapeutic Target for Pulmonary Hypertension.

Uric acid metabolism is implicated in the pathogenesis of pulmonary arterial hypertension, wherein the key metabolite hypoxanthine exhibits elevated levels, thereby promoting pulmonary vascular remodeling through facilitation of cell proliferation and migration as well as regulation of adenosine triphosphate binding cassette transport signaling pathway. Consequently, therapeutic interventions targeting hypoxanthine synthesis may hold promise for the management of pulmonary arterial hypertension.