Document Detail

S-nitrosylation in cardiovascular signaling.
MedLine Citation:
PMID:  20203313     Owner:  NLM     Status:  MEDLINE    
Well over 2 decades have passed since the endothelium-derived relaxation factor was reported to be the gaseous molecule nitric oxide (NO). Although soluble guanylyl cyclase (which generates cyclic guanosine monophosphate, cGMP) was the first identified receptor for NO, it has become increasingly clear that NO exerts a ubiquitous influence in a cGMP-independent manner. In particular, many, if not most, effects of NO are mediated by S-nitrosylation, the covalent modification of a protein cysteine thiol by an NO group to generate an S-nitrosothiol (SNO). Moreover, within the current framework of NO biology, endothelium-derived relaxation factor activity (ie, G protein-coupled receptor-mediated, or shear-induced endothelium-derived NO bioactivity) is understood to involve a central role for SNOs, acting both as second messengers and signal effectors. Furthermore, essential roles for S-nitrosylation have been implicated in virtually all major functions of NO in the cardiovascular system. Here, we review the basic biochemistry of S-nitrosylation (and denitrosylation), discuss the role of S-nitrosylation in the vascular and cardiac functions of NO, and identify current and potential clinical applications.
Brian Lima; Michael T Forrester; Douglas T Hess; Jonathan S Stamler
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Circulation research     Volume:  106     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2010 Mar 
Date Detail:
Created Date:  2010-03-05     Completed Date:  2010-03-26     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  633-46     Citation Subset:  IM    
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MeSH Terms
Cardiovascular Diseases / metabolism*,  pathology,  physiopathology
Cardiovascular System / metabolism*,  pathology,  physiopathology
Cyclic GMP / metabolism
Endothelium, Vascular / metabolism
Endothelium-Dependent Relaxing Factors / metabolism
Inflammation / metabolism
Myocardium / metabolism
Neovascularization, Physiologic
Nitric Oxide / metabolism*
Protein Processing, Post-Translational*
S-Nitrosothiols / metabolism*
Signal Transduction*
Vascular Resistance
Grant Support
P01 HL075443/HL/NHLBI NIH HHS; P01 HL075443-050003/HL/NHLBI NIH HHS; P01-HL075443/HL/NHLBI NIH HHS; R01 HL059130/HL/NHLBI NIH HHS; R01 HL059130-11/HL/NHLBI NIH HHS; R01 HL091876/HL/NHLBI NIH HHS; R01 HL091876-01A1/HL/NHLBI NIH HHS; R01 HL095463/HL/NHLBI NIH HHS; R01 HL095463/HL/NHLBI NIH HHS; R01 HL095463-01A1/HL/NHLBI NIH HHS; R01 HL096673/HL/NHLBI NIH HHS; R01 HL096673-01/HL/NHLBI NIH HHS; R01-HL059130/HL/NHLBI NIH HHS; R01-HL091876/HL/NHLBI NIH HHS; R01-HL096673/HL/NHLBI NIH HHS
Reg. No./Substance:
0/Endothelium-Dependent Relaxing Factors; 0/S-Nitrosothiols; 31C4KY9ESH/Nitric Oxide; H2D2X058MU/Cyclic GMP
Comment In:
Circ Res. 2010 Jul 9;107(1):e1; author reply e2-3   [PMID:  20616330 ]

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