Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander?

Oxidation of low-density lipoprotein (LDL) is thought to contribute to atherosclerosis and cardiovascular disease. Consistent with this idea, the antioxidant drug probucol reduces the risk of restenosis, a form of cardiovascular disease, in humans. However, a new study now suggests that the protecti...

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Detalles Bibliográficos
Autor principal: Heinecke, Jay W.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2006
Materias:
Commentaries
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118281/
https://www.ncbi.nlm.nih.gov/pubmed/16606677
http://dx.doi.org/10.1084/jem.20060218
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author Heinecke, Jay W.
author_facet Heinecke, Jay W.
author_sort Heinecke, Jay W.
collection PubMed
description Oxidation of low-density lipoprotein (LDL) is thought to contribute to atherosclerosis and cardiovascular disease. Consistent with this idea, the antioxidant drug probucol reduces the risk of restenosis, a form of cardiovascular disease, in humans. However, a new study now suggests that the protective effect of probucol depends not on its ability to inhibit lipid oxidation, but on its ability to induce the stress-induced antiinflammatory enzyme heme oxygenase (HO)-1. This might explain why other antioxidants, such as vitamin E, fail to prevent cardiovascular disease in humans.
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spelling pubmed-21182812007-12-13 Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander? Heinecke, Jay W. J Exp Med Commentaries Oxidation of low-density lipoprotein (LDL) is thought to contribute to atherosclerosis and cardiovascular disease. Consistent with this idea, the antioxidant drug probucol reduces the risk of restenosis, a form of cardiovascular disease, in humans. However, a new study now suggests that the protective effect of probucol depends not on its ability to inhibit lipid oxidation, but on its ability to induce the stress-induced antiinflammatory enzyme heme oxygenase (HO)-1. This might explain why other antioxidants, such as vitamin E, fail to prevent cardiovascular disease in humans. The Rockefeller University Press 2006-04-17 /pmc/articles/PMC2118281/ /pubmed/16606677 http://dx.doi.org/10.1084/jem.20060218 Text en Copyright © 2006, The Rockefeller University Press This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Commentaries
Heinecke, Jay W.
Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander?
title Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander?
title_full Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander?
title_fullStr Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander?
title_full_unstemmed Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander?
title_short Lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander?
title_sort lipoprotein oxidation in cardiovascular disease: chief culprit or innocent bystander?
topic Commentaries
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2118281/
https://www.ncbi.nlm.nih.gov/pubmed/16606677
http://dx.doi.org/10.1084/jem.20060218
work_keys_str_mv AT heineckejayw lipoproteinoxidationincardiovasculardiseasechiefculpritorinnocentbystander

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