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Effects of statins on endothelium and signaling mechanisms.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Endres, Matthias Laufs, Ulrich |
| Copyright Year | 2004 |
| 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. |
| Starting Page | 9 |
| Ending Page | 13 |
| Page Count | 5 |
| File Format | PDF HTM / HTML |
| Alternate Webpage(s) | http://stroke.ahajournals.org/content/strokeaha/35/11_suppl_1/2708.full.pdf?download=true |
| Alternate Webpage(s) | http://stroke.ahajournals.org/content/strokeaha/35/11_suppl_1/2708.full.pdf |
| PubMed reference number | 15375300v1 |
| Volume Number | 35 |
| Issue Number | 11 |
| Journal | Stroke |
| Language | English |
| Access Restriction | Open |
| Subject Keyword | 3-hydroxy-3-methylglutaryl-coenzyme A Cholesterol Coenzyme A Coenzymes Endothelium Hydroxymethylglutaryl-CoA reductase Nitric Oxide Synthase Reactive Oxygen Species Simvastatin Superoxides Up-Regulation (Physiology) physical hard work |
| Content Type | Text |
| Resource Type | Article |
