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Recent insights into the cellular biology of atherosclerosis

Atherosclerosis occurs in the subendothelial space (intima) of medium-sized arteries at regions of disturbed blood flow and is triggered by an interplay between endothelial dysfunction and subendothelial lipoprotein retention. Over time, this process stimulates a nonresolving inflammatory response t...

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Detalles Bibliográficos
Autores principales: Tabas, Ira, García-Cardeña, Guillermo, Owens, Gary K.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Rockefeller University Press 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4395483/
https://www.ncbi.nlm.nih.gov/pubmed/25869663
http://dx.doi.org/10.1083/jcb.201412052
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author Tabas, Ira
García-Cardeña, Guillermo
Owens, Gary K.
author_facet Tabas, Ira
García-Cardeña, Guillermo
Owens, Gary K.
author_sort Tabas, Ira
collection PubMed
description Atherosclerosis occurs in the subendothelial space (intima) of medium-sized arteries at regions of disturbed blood flow and is triggered by an interplay between endothelial dysfunction and subendothelial lipoprotein retention. Over time, this process stimulates a nonresolving inflammatory response that can cause intimal destruction, arterial thrombosis, and end-organ ischemia. Recent advances highlight important cell biological atherogenic processes, including mechanotransduction and inflammatory processes in endothelial cells, origins and contributions of lesional macrophages, and origins and phenotypic switching of lesional smooth muscle cells. These advances illustrate how in-depth mechanistic knowledge of the cellular pathobiology of atherosclerosis can lead to new ideas for therapy.
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spelling pubmed-43954832015-10-13 Recent insights into the cellular biology of atherosclerosis Tabas, Ira García-Cardeña, Guillermo Owens, Gary K. J Cell Biol Reviews Atherosclerosis occurs in the subendothelial space (intima) of medium-sized arteries at regions of disturbed blood flow and is triggered by an interplay between endothelial dysfunction and subendothelial lipoprotein retention. Over time, this process stimulates a nonresolving inflammatory response that can cause intimal destruction, arterial thrombosis, and end-organ ischemia. Recent advances highlight important cell biological atherogenic processes, including mechanotransduction and inflammatory processes in endothelial cells, origins and contributions of lesional macrophages, and origins and phenotypic switching of lesional smooth muscle cells. These advances illustrate how in-depth mechanistic knowledge of the cellular pathobiology of atherosclerosis can lead to new ideas for therapy. The Rockefeller University Press 2015-04-13 /pmc/articles/PMC4395483/ /pubmed/25869663 http://dx.doi.org/10.1083/jcb.201412052 Text en © 2015 Tabas et al. 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 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).
spellingShingle Reviews
Tabas, Ira
García-Cardeña, Guillermo
Owens, Gary K.
Recent insights into the cellular biology of atherosclerosis
title Recent insights into the cellular biology of atherosclerosis
title_full Recent insights into the cellular biology of atherosclerosis
title_fullStr Recent insights into the cellular biology of atherosclerosis
title_full_unstemmed Recent insights into the cellular biology of atherosclerosis
title_short Recent insights into the cellular biology of atherosclerosis
title_sort recent insights into the cellular biology of atherosclerosis
topic Reviews
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4395483/
https://www.ncbi.nlm.nih.gov/pubmed/25869663
http://dx.doi.org/10.1083/jcb.201412052
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