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Cell signaling by reactive nitrogen and oxygen species in atherosclerosisThe production of reactive oxygen and nitrogen species has been implicated in atherosclerosis principally as means of damaging low-density lipoprotein that in turn initiates the accumulation of cholesterol in macrophages. The diversity of novel oxidative modifications to lipids and proteins recently identified in atherosclerotic lesions has revealed surprising complexity in the mechanisms of oxidative damage and their potential role in atherosclerosis. Oxidative or nitrosative stress does not completely consume intracellular antioxidants leading to cell death as previously thought. Rather, oxidative and nitrosative stress have a more subtle impact on the atherogenic process by modulating intracellular signaling pathways in vascular tissues to affect inflammatory cell adhesion, migration, proliferation, and differentiation. Furthermore, cellular responses can affect the production of nitric oxide, which in turn can strongly influence the nature of oxidative modifications occurring in atherosclerosis. The dynamic interactions between endogenous low concentrations of oxidants or reactive nitrogen species with intracellular signaling pathways may have a general role in processes affecting wound healing to apoptosis, which can provide novel insights into the pathogenesis of atherosclerosis.
Document ID
20040141441
Acquisition Source
Legacy CDMS
Document Type
Reprint (Version printed in journal)
Authors
Patel, R. P.
(University of Alabama Birmingham, AL 35294-0019, United States)
Moellering, D.
Murphy-Ullrich, J.
Jo, H.
Beckman, J. S.
Darley-Usmar, V. M.
Date Acquired
August 22, 2013
Publication Date
June 15, 2000
Publication Information
Publication: Free radical biology & medicine
Volume: 28
Issue: 12
ISSN: 0891-5849
Subject Category
Life Sciences (General)
Funding Number(s)
CONTRACT_GRANT: HL 50061
CONTRACT_GRANT: DK 54624
CONTRACT_GRANT: HL 58031
Distribution Limits
Public
Copyright
Other
Keywords
Review, Tutorial
Non-NASA Center
NASA Discipline Cell Biology
Review

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