Nitric oxide, oxidative stress, and p66Shc interplay in diabetic endothelial dysfunction

  • Increased oxidative stress and reduced nitric oxide (NO) bioavailability play a causal role in endothelial cell dysfunction occurring in the vasculature of diabetic patients. In this review, we summarized the molecular mechanisms underpinning diabetic endothelial and vascular dysfunction. In particular, we focused our attention on the complex interplay existing among NO, reactive oxygen species (ROS), and one crucial regulator of intracellular ROS production, p66Shc protein.

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Metadaten
Author:Alessandra Magenta, Simona Greco, Maurizio C. Capogrossi, Carlo Gaetano, Fabio Martelli
URN:urn:nbn:de:hebis:30:3-334705
DOI:https://doi.org/10.1155/2014/193095
ISSN:2314-6133
ISSN:2314-6141
Pubmed Id:https://pubmed.ncbi.nlm.nih.gov/24734227
Parent Title (English):BioMed research international
Publisher:Hindawi
Place of publication:New York, NY [u.a.]
Document Type:Article
Language:English
Date of Publication (online):2014/03/05
Date of first Publication:2014/03/05
Publishing Institution:Universitätsbibliothek Johann Christian Senckenberg
Release Date:2014/05/23
Volume:2014
Issue:Article ID 193095
Page Number:16
Note:
Copyright © 2014 Alessandra Magenta et al. This is an open access article distributed under the Creative Commons Attribution License http://creativecommons.org/licenses/by/3.0/ , which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
HeBIS-PPN:365069892
Institutes:Medizin / Medizin
Dewey Decimal Classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Sammlungen:Universitätspublikationen
Licence (German):License LogoCreative Commons - Namensnennung 3.0