Literature DB >> 28190244

NADPH oxidase: its potential role in promotion of pulmonary arterial hypertension.

Jing-Jie Peng1,2, Bin Liu1,3, Jin-Yun Xu2, Jun Peng4,5, Xiu-Ju Luo6.   

Abstract

NADPH oxidases (NOXs) are a group of enzymes for superoxide anion (O2·- ) generation through transferring electrons from NADPH to molecular oxygen, which is rapidly converted into hydrogen peroxide (H2O2). There are seven members in NOX family, including NOX1 to NOX5, dual oxidase1, and dual oxidase 2. Recent studies have demonstrated that NOX subtypes may have different functions in different types of pulmonary arterial hypertension (PAH). The NOX-derived reactive oxygen species (ROS) are key factors that are involved in promoting the processes of pulmonary vascular remodeling, such as endothelial dysfunction, proliferation of pulmonary arterial smooth muscle cells (PASMCs), and cellular trans-differentiation, which are the basic pathologic characteristics of PAH. Inhibition of NOX shows beneficial effect on prevention of PAH development. Thus, NOX might be a potential target for PAH therapy. The main purpose of this review is to summarize recent findings on the role of NOX, particularly the NOX subtypes, in promotion of PAH development and to list recent progress regarding the NOX-based intervention for PAH.

Entities:  

Keywords:  Apocynin; Diphenyleneiodonium; NADPH oxidases; Pulmonary arterial hypertension; Resveratrol

Mesh:

Substances:

Year:  2017        PMID: 28190244     DOI: 10.1007/s00210-017-1359-2

Source DB:  PubMed          Journal:  Naunyn Schmiedebergs Arch Pharmacol        ISSN: 0028-1298            Impact factor:   3.000


  65 in total

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Journal:  Am J Physiol Lung Cell Mol Physiol       Date:  2011-12-23       Impact factor: 5.464

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8.  Inhibition of NOX/VPO1 pathway and inflammatory reaction by trimethoxystilbene in prevention of cardiovascular remodeling in hypoxia-induced pulmonary hypertensive rats.

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Review 9.  Small-molecule NOX inhibitors: ROS-generating NADPH oxidases as therapeutic targets.

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Journal:  BMC Evol Biol       Date:  2007-09-27       Impact factor: 3.260

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