Effects of statins on endothelium and signaling mechanisms.

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

Stroke

journal_title

Stroke

authors

Endres M,Laufs U

doi

10.1161/01.STR.0000143319.73503.38

subject

Has Abstract

pub_date

2004-11-01 00:00:00

pages

2708-11

issue

11 Suppl 1

eissn

0039-2499

issn

1524-4628

pii

01.STR.0000143319.73503.38

journal_volume

35

pub_type

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