NADPH Oxidase–Mediated ROS in Pulmonary Arterial Hypertension

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Antioxidant Enzyme Systems".

Deadline for manuscript submissions: closed (31 January 2019) | Viewed by 9224

Special Issue Editor


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Guest Editor
Department of Pharmacology and Toxicology, Medical College of Georgia, Augusta University, 1460 Laney Walker Blvd, CB3626, Augusta, GA 30912, USA
Interests: reactive oxygen species (ROS); NADPH oxidase; Galectin-3; PAH; vascular remodeling; redox signaling; adventitia; inflammation; vascular biology

Special Issue Information

Dear Colleagues,

Pulmonary arterial hypertension (PAH) is a progressive disease that involves the loss of endothelial function together with aberrant smooth muscle cell growth, inflammation, and fibrosis that involves multiple cell types in the pulmonary arteries (PA). How PAH develops remains incompletely understood, but evidence for production of reactive oxygen species (ROS) in PA has been well documented. There are many different types of ROS with multiple sources that may contribute to the pulmonary arterial remodeling that is a hallmark of PAH. The NADPH oxidase (Nox) family is comprised of seven structurally related transmembrane NADPH-dependent oxidoreductases that include the Nox enzymes, as well as the Duoxes. Accumulating evidence strongly suggests that ROS derived from NADPH oxidase play an important role in pulmonary arterial remodeling. The signaling mechanisms leading to activation of the Nox enzymes are diverse, and more precise targeting of the major sources of ROS in specific cell types in PA will likely be more effective towards development of therapeutic treatments for PAH.

The goal of this Special Issue is to bring together and outline the current state and importance of the role of NADPH oxidases in the context of PAH. Suppressing pathophysiological levels of ROS by manipulating NOX enzymes, their regulators, and effector ROS targets appears to be attractive therapeutic strategies to treat PAH and other related pulmonary vascular diseases. This Special Issue invites original research and review articles on the subject of NADPH-oxidases in the context of pulmonary vascular pathophysiology and all the related topics indicated below:

Prof. Scott A. Barman
Guest Editor

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Keywords

  • Reactive Oxygen Species 
  • Inflammation 
  • Pulmonary Arterial Hypertension 
  • Redox Signaling 
  • Endothelial Cell 
  • Pulmonary Arterial Remodeling 
  • Adventitia 
  • Fibrosis

Published Papers (2 papers)

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Review

30 pages, 2810 KiB  
Review
Role of Gender in Regulation of Redox Homeostasis in Pulmonary Arterial Hypertension
by Ruslan Rafikov, Joel James, Nolan McClain, Stevan P. Tofovic and Olga Rafikova
Antioxidants 2019, 8(5), 135; https://doi.org/10.3390/antiox8050135 - 16 May 2019
Cited by 10 | Viewed by 4691
Abstract
Pulmonary arterial hypertension (PAH) is one of the diseases with a well-established gender dimorphism. The prevalence of PAH is increased in females with a ratio of 4:1, while poor survival prognosis is associated with the male gender. Nevertheless, the specific contribution of gender [...] Read more.
Pulmonary arterial hypertension (PAH) is one of the diseases with a well-established gender dimorphism. The prevalence of PAH is increased in females with a ratio of 4:1, while poor survival prognosis is associated with the male gender. Nevertheless, the specific contribution of gender in disease development and progression is unclear due to the complex nature of the PAH. Oxidative and nitrosative stresses are important contributors in PAH pathogenesis; however, the role of gender in redox homeostasis has been understudied. This review is aimed to overview the possible sex-specific mechanisms responsible for the regulation of the balance between oxidants and antioxidants in relation to PAH pathobiology. Full article
(This article belongs to the Special Issue NADPH Oxidase–Mediated ROS in Pulmonary Arterial Hypertension)
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14 pages, 656 KiB  
Review
Regulation of Smooth Muscle Cell Proliferation by NADPH Oxidases in Pulmonary Hypertension
by John C. Huetsch, Karthik Suresh and Larissa A. Shimoda
Antioxidants 2019, 8(3), 56; https://doi.org/10.3390/antiox8030056 - 05 Mar 2019
Cited by 24 | Viewed by 4166
Abstract
Hyperproliferation of pulmonary arterial smooth muscle cells is a key component of vascular remodeling in the setting of pulmonary hypertension (PH). Numerous studies have explored factors governing the changes in smooth muscle cell phenotype that lead to the increased wall thickness, and have [...] Read more.
Hyperproliferation of pulmonary arterial smooth muscle cells is a key component of vascular remodeling in the setting of pulmonary hypertension (PH). Numerous studies have explored factors governing the changes in smooth muscle cell phenotype that lead to the increased wall thickness, and have identified various potential candidates. A role for reactive oxygen species (ROS) has been well documented in PH. ROS can be generated from a variety of sources, including mitochondria, uncoupled nitric oxide synthase, xanthine oxidase, and reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. In this article, we will review recent data supporting a role for ROS generated from NADPH oxidases in promoting pulmonary arterial smooth muscle cell proliferation during PH. Full article
(This article belongs to the Special Issue NADPH Oxidase–Mediated ROS in Pulmonary Arterial Hypertension)
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