Effect of Tryptophan Hydroxylase 1 Deficiency on the Development of Hypoxia-Induced Pulmonary Hypertension (original) (raw)

Pulmonary arterial hypertension (PAH) is a serious condition often linked to genetic factors, including mutations affecting serotonin transport and production. This study investigates the impact of Tryptophan Hydroxylase 1 (Tph1) deficiency on the development of hypoxia-induced PAH in mice. Findings demonstrate that Tph1-deficient mice show reduced pulmonary vascular remodeling and lower pulmonary pressure in a hypoxic environment. These results highlight the role of peripheral serotonin in PAH and suggest that targeting Tph1 could offer a new therapeutic strategy for managing this disease.