Role of oxidized lipids in pulmonary arterial hypertension

Abstract

Pulmonary arterial hypertension (PAH) is a multifactorial disease characterized by interplay of many cellular, molecular, and genetic events that lead to excessive proliferation of pulmonary cells, including smooth muscle and endothelial cells; inflammation; and extracellular matrix remodeling. Abnormal vascular changes and structural remodeling associated with PAH culminate in vasoconstriction and obstruction of pulmonary arteries, contributing to increased pulmonary vascular resistance, pulmonary hypertension, and right ventricular failure. The complex molecular mechanisms involved in the pathobiology of PAH are the limiting factors in the development of potential therapeutic interventions for PAH. Over the years, our group and others have demonstrated the critical implication of lipids in the pathogenesis of PAH. This review specifically focuses on the current understanding of the role of oxidized lipids, lipid metabolism, peroxidation, and oxidative stress in the progression of PAH. This review also discusses the relevance of apolipoprotein A-I mimetic peptides and microRNA-193, which are known to regulate the levels of oxidized lipids, as potential therapeutics in PAH.

Read the full article online

Topics

Oxidative stress and Oxidants/Antioxidants and Free Radicals
Pulmonary Hypertension

Authors

Salil Sharma, Grégoire Ruffenach, Soban Umar, Negar Motayagheni, Srinivasa T. Reddy, and Mansoureh Eghbali

Published in:

Pulmonary Circulation Vol 6: No 3 cover image

September 2016

Pulmonary Circulation Vol 6: No 3

View this journal

Our research platform is the world.

Through worldwide collaboration, we can begin to answer the question of a global disease.

Join the PVRI
standard-example-image.jpg