Document Detail


Reactive oxygen species in pulmonary vascular remodeling.
MedLine Citation:
PMID:  23897679     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The pathogenesis of pulmonary hypertension is a complex multifactorial process that involves the remodeling of pulmonary arteries. This remodeling process encompasses concentric medial thickening of small arterioles, neomuscularization of previously nonmuscular capillary-like vessels, and structural wall changes in larger pulmonary arteries. The pulmonary arterial muscularization is characterized by vascular smooth muscle cell hyperplasia and hypertrophy. In addition, in uncontrolled pulmonary hypertension, the clonal expansion of apoptosis-resistant endothelial cells leads to the formation of plexiform lesions. Based upon a large number of studies in animal models, the three major stimuli that drive the vascular remodeling process are inflammation, shear stress, and hypoxia. Although, the precise mechanisms by which these stimuli impair pulmonary vascular function and structure are unknown, reactive oxygen species (ROS)-mediated oxidative damage appears to play an important role. ROS are highly reactive due to their unpaired valence shell electron. Oxidative damage occurs when the production of ROS exceeds the quenching capacity of the antioxidant mechanisms of the cell. ROS can be produced from complexes in the cell membrane (nicotinamide adenine dinucleotide phosphate-oxidase), cellular organelles (peroxisomes and mitochondria), and in the cytoplasm (xanthine oxidase). Furthermore, low levels of tetrahydrobiopterin (BH4) and L-arginine the rate limiting cofactor and substrate for endothelial nitric oxide synthase (eNOS), can cause the uncoupling of eNOS, resulting in decreased NO production and increased ROS production. This review will focus on the ROS generation systems, scavenger antioxidants, and oxidative stress associated alterations in vascular remodeling in pulmonary hypertension.
Authors:
Saurabh Aggarwal; Christine M Gross; Shruti Sharma; Jeffrey R Fineman; Stephen M Black
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Comprehensive Physiology     Volume:  3     ISSN:  2040-4603     ISO Abbreviation:  Compr Physiol     Publication Date:  2013 Jul 
Date Detail:
Created Date:  2013-07-30     Completed Date:  2013-11-19     Revised Date:  2014-07-02    
Medline Journal Info:
Nlm Unique ID:  101574442     Medline TA:  Compr Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1011-34     Citation Subset:  IM    
Copyright Information:
© 2013 American Physiological Society.
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MeSH Terms
Descriptor/Qualifier:
Adaptation, Physiological / physiology
Animals
Antioxidants / therapeutic use
Disease Models, Animal
Free Radical Scavengers / metabolism
Humans
Hypertension, Pulmonary / drug therapy,  physiopathology*
Oxidative Stress / physiology
Reactive Oxygen Species / metabolism*
Grant Support
ID/Acronym/Agency:
HD057406/HD/NICHD NIH HHS; HL084739/HL/NHLBI NIH HHS; HL60190/HL/NHLBI NIH HHS; HL61284/HL/NHLBI NIH HHS; HL67841/HL/NHLBI NIH HHS; P01 HL101902/HL/NHLBI NIH HHS; R01 HL060190/HL/NHLBI NIH HHS; R01 HL061284/HL/NHLBI NIH HHS; R01 HL067841/HL/NHLBI NIH HHS; R01 HL084739/HL/NHLBI NIH HHS; R21 HD057406/HD/NICHD NIH HHS
Chemical
Reg. No./Substance:
0/Antioxidants; 0/Free Radical Scavengers; 0/Reactive Oxygen Species
Comments/Corrections

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