Regulation of endothelial derived nitric oxide in health and disease

Memórias do Instituto Oswaldo Cruz

William C Sessa¹ 

[1] ,Yale University School of Medicine Boyer Center for Molecular MedicineNew Haven CT ,US

关键词: nitric oxide;    endothelium;    caveolin-1;    heat shock protein 90;    atherosclerosis;    inflammation;   

DOI  :  10.1590/S0074-02762005000900004

来源: SciELO

【 摘 要 】

Endothelial nitric oxide synthase (eNOS) is the primary physiological source of nitric oxide (NO) that regulates cardiovascular homeostasis. Historically eNOS has been thought to be a constitutively expressed enzyme regulated by calcium and calmodulin. However, in the last five years it is clear that eNOS activity and NO release can be regulated by post-translational control mechanisms (fatty acid modification and phosphorylation) and protein-protein interactions (with caveolin-1 and heat shock protein 90) that direct impinge upon the duration and magnitude of NO release. This review will summarize this information and apply the post-translational control mechanisms to disease states.

【 授权许可】

CC BY   
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