期刊
ANTIOXIDANTS & REDOX SIGNALING
卷 8, 期 9-10, 页码 1693-1705出版社
MARY ANN LIEBERT, INC
DOI: 10.1089/ars.2006.8.1693
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资金
- NATIONAL HEART, LUNG, AND BLOOD INSTITUTE [R01HL039752] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ENVIRONMENTAL HEALTH SCIENCES [Z01ES101565, Z01ES100327, Z01ES010004] Funding Source: NIH RePORTER
- NHLBI NIH HHS [R01 HL039752] Funding Source: Medline
Nitric oxide (NO) plays an important role in the regulation of cardiovascular function. S-nitrosylation, the covalent attachment of an NO moiety to sulfhydryl residues of proteins, resulting in the formation of S-nitrosothiols (SNOs), is a prevalent posttranslational protein modification involved in redox-based cellular signaling. Under physiologic conditions, protein S-nitrosylation and SNOs provide protection preventing further cellular oxidative and nitrosative stress. However, oxidative stress and the resultant dysfunction of NO signaling have been implicated in the pathogenesis of cardiovascular diseases.
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