Key result
Targeting nitric oxide, oxidative stress, and inflammation offers key therapeutic pathways in pulmonary arterial hypertension.
Understanding the interconnected roles of nitric oxide, oxidative stress, and inflammation in PAH pathogenesis is crucial for developing effective, multi-targeted therapeutic strategies.
Pulmonary arterial hypertension (PAH) is a chronic and progressive disease characterized by a persistent elevation of pulmonary artery pressure accompanied by right ventricular hypertrophy (RVH). The current treatment for pulmonary hypertension is limited and only provides symptomatic relief due to unknown cause and pathogenesis of the disease. Both vasoconstriction and structural remodeling (enhanced proliferation of vascular smooth muscle cell) of the pulmonary arteries contribute to the progressive course of PAH, irrespective of different underlying causes. The exact molecular mechanism of PAH, however, is not fully understood. The purpose of this review is to provide recent advances in the mechanistic investigation of PAH. Specifically, this review focuses on nitric oxide, oxidative stress and inflammation and how these factors contribute to the development and progression of PAH. This review also discusses recent and potential therapeutic advancements for the treatment of PAH.
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Crosswhite et al. (2010) conducted a review in Pulmonary arterial hypertension. Therapeutics targeting nitric oxide, oxidative stress, and inflammation was evaluated. Nitric oxide, oxidative stress, and inflammation play critical, interconnected roles in the pathogenesis of pulmonary arterial hypertension and serve as targets for current and emerging therapies.
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