Reactive Oxygen and Nitrogen Species in the Development of Pulmonary Hypertension

David J R Fulton; Xueyi Li; Zsuzsanna Bordan; Stephen Haigh; Austin Bentley; Feng Chen; Scott A Barman

doi:10.3390/antiox6030054

Reactive Oxygen and Nitrogen Species in the Development of Pulmonary Hypertension

Antioxidants (Basel). 2017 Jul 6;6(3):54. doi: 10.3390/antiox6030054.

Authors

David J R Fulton¹, Xueyi Li², Zsuzsanna Bordan³, Stephen Haigh⁴, Austin Bentley⁵, Feng Chen⁶, Scott A Barman⁷

Affiliations

¹ Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. DFULTON@augusta.edu.
² Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. xuli@augusta.edu.
³ Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. zbordan@augusta.edu.
⁴ Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. shaigh@augusta.edu.
⁵ Vascular Biology Center, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. aubentley@augusta.edu.
⁶ Department of Forensic Medicine, Nanjing Medical University, Nanjing 211166, China. fchen@njmu.edu.cn.
⁷ Department of Pharmacology and Toxicology, Medical College of Georgia at Augusta University, Augusta, GA 30912, USA. sbarman@augusta.edu.

Abstract

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.

Keywords: Nox; endothelial nitric oxide synthase (eNOS); nicotinamide adenine dinucleotide phosphate-oxidase (NADPH oxidase); nitric oxide; pulmonary hypertension; reactive oxygen species.

Publication types

Review

Abstract

Publication types

Grants and funding