STAT1 as a central mediator of IFNγ and TLR4 signal integration in vascular dysfunction

Atherosclerosis is characterized by early endothelial dysfunction and altered vascular smooth muscle cells (VSMCs) contractility. The forming atheroma is a site of excessive production of cytokines and inflammatory ligands by various cell types that mediate inflammation and immune responses. Key fac...

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Autores principales: Sikorski, Krzysztof, Chmielewski, Stefan, Olejnik, Adam, Wesoly, Joanna Z., Heemann, Uwe, Baumann, Marcus, Bluyssen, Hans
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Landes Bioscience 2012
Materias:
Review
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670280/
https://www.ncbi.nlm.nih.gov/pubmed/24058779
http://dx.doi.org/10.4161/jkst.22469
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author Sikorski, Krzysztof
Chmielewski, Stefan
Olejnik, Adam
Wesoly, Joanna Z.
Heemann, Uwe
Baumann, Marcus
Bluyssen, Hans
author_facet Sikorski, Krzysztof
Chmielewski, Stefan
Olejnik, Adam
Wesoly, Joanna Z.
Heemann, Uwe
Baumann, Marcus
Bluyssen, Hans
author_sort Sikorski, Krzysztof
collection PubMed
description Atherosclerosis is characterized by early endothelial dysfunction and altered vascular smooth muscle cells (VSMCs) contractility. The forming atheroma is a site of excessive production of cytokines and inflammatory ligands by various cell types that mediate inflammation and immune responses. Key factors contributing to early stages of plaque development are IFNγ and TLR4. This review provides insight in the differential STAT1-dependent signal integration between IFNγ and TLR4 signals in vascular cells and atheroma interacting immune cells. This results in increased leukocyte attraction and adhesion and VSMC proliferation and migration, which are important characteristics of EC dysfunction and early triggers of atherosclerosis.
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spelling pubmed-36702802013-09-19 STAT1 as a central mediator of IFNγ and TLR4 signal integration in vascular dysfunction Sikorski, Krzysztof Chmielewski, Stefan Olejnik, Adam Wesoly, Joanna Z. Heemann, Uwe Baumann, Marcus Bluyssen, Hans JAKSTAT Review Atherosclerosis is characterized by early endothelial dysfunction and altered vascular smooth muscle cells (VSMCs) contractility. The forming atheroma is a site of excessive production of cytokines and inflammatory ligands by various cell types that mediate inflammation and immune responses. Key factors contributing to early stages of plaque development are IFNγ and TLR4. This review provides insight in the differential STAT1-dependent signal integration between IFNγ and TLR4 signals in vascular cells and atheroma interacting immune cells. This results in increased leukocyte attraction and adhesion and VSMC proliferation and migration, which are important characteristics of EC dysfunction and early triggers of atherosclerosis. Landes Bioscience 2012-10-01 2012-10-01 /pmc/articles/PMC3670280/ /pubmed/24058779 http://dx.doi.org/10.4161/jkst.22469 Text en Copyright © 2012 Landes Bioscience http://creativecommons.org/licenses/by-nc/3.0/ This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Review
Sikorski, Krzysztof
Chmielewski, Stefan
Olejnik, Adam
Wesoly, Joanna Z.
Heemann, Uwe
Baumann, Marcus
Bluyssen, Hans
STAT1 as a central mediator of IFNγ and TLR4 signal integration in vascular dysfunction
title STAT1 as a central mediator of IFNγ and TLR4 signal integration in vascular dysfunction
title_full STAT1 as a central mediator of IFNγ and TLR4 signal integration in vascular dysfunction
title_fullStr STAT1 as a central mediator of IFNγ and TLR4 signal integration in vascular dysfunction
title_full_unstemmed STAT1 as a central mediator of IFNγ and TLR4 signal integration in vascular dysfunction
title_short STAT1 as a central mediator of IFNγ and TLR4 signal integration in vascular dysfunction
title_sort stat1 as a central mediator of ifnγ and tlr4 signal integration in vascular dysfunction
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3670280/
https://www.ncbi.nlm.nih.gov/pubmed/24058779
http://dx.doi.org/10.4161/jkst.22469
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