Document Detail


Reactive oxygen and nitrogen species in pulmonary hypertension.
MedLine Citation:
PMID:  22401856     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pulmonary vascular disease can be defined as either a disease affecting the pulmonary capillaries and pulmonary arterioles, termed pulmonary arterial hypertension, or a disease affecting the left ventricle, called pulmonary venous hypertension. Pulmonary arterial hypertension (PAH) is a disorder of the pulmonary circulation characterized by endothelial dysfunction, as well as intimal and smooth muscle proliferation. Progressive increases in pulmonary vascular resistance and pressure impair the performance of the right ventricle, resulting in declining cardiac output, reduced exercise capacity, right-heart failure, and ultimately death. While the primary and heritable forms of the disease are thought to affect over 5000 patients in the United States, the disease can occur secondary to congenital heart disease, most advanced lung diseases, and many systemic diseases. Multiple studies implicate oxidative stress in the development of PAH. Further, this oxidative stress has been shown to be associated with alterations in reactive oxygen species (ROS), reactive nitrogen species (RNS), and nitric oxide (NO) signaling pathways, whereby bioavailable NO is decreased and ROS and RNS production are increased. Many canonical ROS and NO signaling pathways are simultaneously disrupted in PAH, with increased expression of nicotinamide adenine dinucleotide phosphate (NADPH) oxidases and xanthine oxidoreductase, uncoupling of endothelial NO synthase (eNOS), and reduction in mitochondrial number, as well as impaired mitochondrial function. Upstream dysregulation of ROS/NO redox homeostasis impairs vascular tone and contributes to the pathological activation of antiapoptotic and mitogenic pathways, leading to cell proliferation and obliteration of the vasculature. This paper will review the available data regarding the role of oxidative and nitrosative stress and endothelial dysfunction in the pathophysiology of pulmonary hypertension, and provide a description of targeted therapies for this disease.
Authors:
Diana M Tabima; Sheila Frizzell; Mark T Gladwin
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2012-03-06
Journal Detail:
Title:  Free radical biology & medicine     Volume:  52     ISSN:  1873-4596     ISO Abbreviation:  Free Radic. Biol. Med.     Publication Date:  2012 May 
Date Detail:
Created Date:  2012-05-01     Completed Date:  2012-09-28     Revised Date:  2013-12-17    
Medline Journal Info:
Nlm Unique ID:  8709159     Medline TA:  Free Radic Biol Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1970-86     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Humans
Hypertension, Pulmonary / metabolism*
Reactive Nitrogen Species / metabolism*
Reactive Oxygen Species / metabolism*
Grant Support
ID/Acronym/Agency:
P01 HL103455/HL/NHLBI NIH HHS; P01HL103455/HL/NHLBI NIH HHS; R01 HL096973/HL/NHLBI NIH HHS; R01 HL098032/HL/NHLBI NIH HHS; R01HL096973/HL/NHLBI NIH HHS; R01HL098032/HL/NHLBI NIH HHS; RC1 DK085852/DK/NIDDK NIH HHS; RC1DK085852/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Reactive Nitrogen Species; 0/Reactive Oxygen Species
Comments/Corrections

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