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  • Endothelial nitric oxide (NO) and its pathophysiologic regulation
  • Chatterjee A; Black SM; Catravas JD
  • Vascul Pharmacol 2008[Oct]; 49 (4-6): 134-40
  • Nitric oxide (NO) is a gaseous lipophilic free radical generated by three distinct isoforms of nitric oxide synthases (NOS), type 1 or neuronal (nNOS), type 2 or inducible (iNOS) and type 3 or endothelial NOS (eNOS). Expression of eNOS is altered in many types of cardiovascular disease, such as atherosclerosis, diabetes and hypertension. The ubiquitous chaperone heat shock protein 90 (hsp90) associates with NOS and is important for its proper folding and function. Current studies point toward a therapeutic potential by modulating hsp90-NOS association in various vascular diseases. Here we review the transcriptional regulation of endothelial NOS and factors affecting eNOS activity and function, as well as the important vascular pathologies associated with altered NOS function, focusing on the regulatory role of hsp90 and other factors in NO-associated pathogenesis of these diseases.
  • |Animals[MESH]
  • |Endothelium, Vascular/metabolism/*physiopathology[MESH]
  • |Gene Expression Regulation, Enzymologic[MESH]
  • |HSP90 Heat-Shock Proteins/metabolism[MESH]
  • |Humans[MESH]
  • |Nitric Oxide Synthase Type III/genetics/*metabolism[MESH]
  • |Nitric Oxide/biosynthesis/*physiology[MESH]
  • |Vascular Diseases/metabolism/*physiopathology[MESH]

  • *{{pmid18692595}}
    *<b>[ Endothelial nitric oxide (NO) and its pathophysiologic regulation ]</b> Vascul Pharmacol 2008; 49(4-6) ; 134-40 Chatterjee A; Black SM; Catravas JD


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    Vascul Pharmacol

    134 4-6.49 2008