Pleiotropic effects of statins in stroke prevention

Cardiovascular disease is the leading cause of death and disability, and contributes substantially to healthcare budgets. The lipid-lowering drugs, 3-hydroxy-3-methylgulutaryl-coenzyme A (HMG-CoA) reductase inhibitor or statins, reducing mortality and cardiovascular morbidity in patients with estab...

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Main Author: Yenny
Format: Article
Language:English
Published: Faculty of Medicine Trisakti University 2009-08-01
Series:Universa Medicina
Subjects:
Online Access:http://www.univmed.org/wp-content/uploads/2011/02/Yenny1(3).pdf
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spelling doaj-70ba71d53def4f2b9be7bf1811caeedb2020-11-25T03:15:28ZengFaculty of Medicine Trisakti UniversityUniversa Medicina1907-30622009-08-01282117126Pleiotropic effects of statins in stroke preventionYenny0Department of Pharmacology Medical Faculty, Trisakti University, JakartaCardiovascular disease is the leading cause of death and disability, and contributes substantially to healthcare budgets. The lipid-lowering drugs, 3-hydroxy-3-methylgulutaryl-coenzyme A (HMG-CoA) reductase inhibitor or statins, reducing mortality and cardiovascular morbidity in patients with established cardiovascular disease. Statins therefore have a place in the secondary prevention of cardiovascular disease. Recent experimental and clinical studies suggest that statins may exert vascular protective effect beyond cholesterol reduction. The cholesterol-independet or “pleiotropic” effects of statin include the upregulation and activation of endothelial nitric acid synthase (eNOS) that can increase nitric oxide (NO) production. Augmentation of NO production increases cerebral blood flow, which can lead to neuroprotection during brain ischaemia. By inhibiting mevalonate synthesis, statins prevent the formation of several isoprenoids (including farnesylpyrophosphate and geranylgeranylpyrophosphate). Inhibiting geranylgeranylation of RhoA small G proteins increases the stability of eNOS mRNA through the remodeling of endothelial actin microfilamens. Moreover, statins directly increase eNOS activity within minutes by activating the pathway involving phosphoinositide 3-kinase and protein kinase B. In the secondary prevention of stroke, the use of statins reduces the incidence of either recurrent stroke or other major vascular events and treatment should be initiated soon after the event. The use of statins does not increase hemorrhagic stroke or cancer and may also favor atherosclerotic plaque regression.http://www.univmed.org/wp-content/uploads/2011/02/Yenny1(3).pdfStatinendothelial nitric synthase stroke ischemic
collection DOAJ
language English
format Article
sources DOAJ
author Yenny
spellingShingle Yenny
Pleiotropic effects of statins in stroke prevention
Universa Medicina
Statin
endothelial nitric synthase stroke ischemic
author_facet Yenny
author_sort Yenny
title Pleiotropic effects of statins in stroke prevention
title_short Pleiotropic effects of statins in stroke prevention
title_full Pleiotropic effects of statins in stroke prevention
title_fullStr Pleiotropic effects of statins in stroke prevention
title_full_unstemmed Pleiotropic effects of statins in stroke prevention
title_sort pleiotropic effects of statins in stroke prevention
publisher Faculty of Medicine Trisakti University
series Universa Medicina
issn 1907-3062
publishDate 2009-08-01
description Cardiovascular disease is the leading cause of death and disability, and contributes substantially to healthcare budgets. The lipid-lowering drugs, 3-hydroxy-3-methylgulutaryl-coenzyme A (HMG-CoA) reductase inhibitor or statins, reducing mortality and cardiovascular morbidity in patients with established cardiovascular disease. Statins therefore have a place in the secondary prevention of cardiovascular disease. Recent experimental and clinical studies suggest that statins may exert vascular protective effect beyond cholesterol reduction. The cholesterol-independet or “pleiotropic” effects of statin include the upregulation and activation of endothelial nitric acid synthase (eNOS) that can increase nitric oxide (NO) production. Augmentation of NO production increases cerebral blood flow, which can lead to neuroprotection during brain ischaemia. By inhibiting mevalonate synthesis, statins prevent the formation of several isoprenoids (including farnesylpyrophosphate and geranylgeranylpyrophosphate). Inhibiting geranylgeranylation of RhoA small G proteins increases the stability of eNOS mRNA through the remodeling of endothelial actin microfilamens. Moreover, statins directly increase eNOS activity within minutes by activating the pathway involving phosphoinositide 3-kinase and protein kinase B. In the secondary prevention of stroke, the use of statins reduces the incidence of either recurrent stroke or other major vascular events and treatment should be initiated soon after the event. The use of statins does not increase hemorrhagic stroke or cancer and may also favor atherosclerotic plaque regression.
topic Statin
endothelial nitric synthase stroke ischemic
url http://www.univmed.org/wp-content/uploads/2011/02/Yenny1(3).pdf
work_keys_str_mv AT yenny pleiotropiceffectsofstatinsinstrokeprevention
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