Key result
Reactive oxygen and nitrogen species drive pathogenesis in pulmonary hypertension via Nox and uncoupled eNOS.
This review highlights the pathophysiological role of reactive oxygen and nitrogen species in driving endothelial dysfunction and vascular remodeling in pulmonary arterial hypertension.
No practice change for pulmonary hypertension; leaves open targeted trials on oxidative pathways.
Pulmonary arterial hypertension (PAH) is a progressive disease of the lung vasculature that involves the loss of endothelial function together with inappropriate smooth muscle cell growth, inflammation, and fibrosis. These changes underlie a progressive remodeling of blood vessels that alters flow and increases pulmonary blood pressure. Elevated pressures in the pulmonary artery imparts a chronic stress on the right ventricle which undergoes compensatory hypertrophy but eventually fails. How PAH develops remains incompletely understood and evidence for the altered production of reactive oxygen and nitrogen species (ROS, RNS respectively) in the pulmonary circulation has been well documented. There are many different types of ROS and RNS, multiple sources, and collective actions and interactions. This review summarizes past and current knowledge of the sources of ROS and RNS and how they may contribute to the loss of endothelial function and changes in smooth muscle proliferation in the pulmonary circulation.
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Fulton et al. (2017) conducted a review in Pulmonary Hypertension. Reactive Oxygen and Nitrogen Species (ROS and RNS) was evaluated. Reactive oxygen and nitrogen species derived from multiple enzymatic sources, including Nox enzymes and uncoupled eNOS, play a critical role in the pathogenesis of pulmonary hypertension.
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