Abstract:
:Endothelium dysfunction may result from increased production of reactive oxygen species and decreased availability of nitric oxide. Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (ie, statins) exert cholesterol-independent vasoprotective effects that are mediated, in part, through the inhibition of small G-proteins Rho and Rac. Rho negatively regulates endothelial nitric oxide synthase and Rac contributes to NAD(P)H-oxidase activation and superoxide production. Statins inhibit both Rho and Rac GTPase activity via inhibition of geranylgeranylation, which confers endothelial nitric oxide synthase upregulation and decreases superoxide production, respectively. Sudden discontinuation of statin therapy may have negative effects. Withdrawal of statin treatment leads to an overshoot activation of Rho and Rac with dramatic effects on nitric oxide bioavailability, NAD(P)H-oxidase activity, and superoxide production.
journal_name
Strokejournal_title
Strokeauthors
Endres M,Laufs Udoi
10.1161/01.STR.0000143319.73503.38subject
Has Abstractpub_date
2004-11-01 00:00:00pages
2708-11issue
11 Suppl 1eissn
0039-2499issn
1524-4628pii
01.STR.0000143319.73503.38journal_volume
35pub_type
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