Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury

Anna Uryga and Mandy Grootaert et al. combine cell culture and animal models to examine how senescence of human vascular smooth muscle cells (VSMCs) and persistent telomere damage drive inflammation. Their results suggest that telomere injury can be the primary cause of premature senescence in VSMCs...

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Autores principales:	Anna K. Uryga, Mandy O. J. Grootaert, Abel M. Garrido, Sebnem Oc, Kirsty Foote, Joel Chappell, Alison Finigan, Francesca Rossiello, Fabrizio d’Adda di Fagagna, Dimitra Aravani, Helle F. Jorgensen, Martin R. Bennett
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2021
Materias:	Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/89fb7bb2970a4e30ac925d9236fd3bc3
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spelling	oai:doaj.org-article:89fb7bb2970a4e30ac925d9236fd3bc32021-12-02T15:52:54ZTelomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury10.1038/s42003-021-02123-z2399-3642https://doaj.org/article/89fb7bb2970a4e30ac925d9236fd3bc32021-05-01T00:00:00Zhttps://doi.org/10.1038/s42003-021-02123-zhttps://doaj.org/toc/2399-3642Anna Uryga and Mandy Grootaert et al. combine cell culture and animal models to examine how senescence of human vascular smooth muscle cells (VSMCs) and persistent telomere damage drive inflammation. Their results suggest that telomere injury can be the primary cause of premature senescence in VSMCs, and that DNA damage can be a major cause of persistent inflammation in vascular disease.Anna K. UrygaMandy O. J. GrootaertAbel M. GarridoSebnem OcKirsty FooteJoel ChappellAlison FiniganFrancesca RossielloFabrizio d’Adda di FagagnaDimitra AravaniHelle F. JorgensenMartin R. BennettNature PortfolioarticleBiology (General)QH301-705.5ENCommunications Biology, Vol 4, Iss 1, Pp 1-16 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biology (General) QH301-705.5
spellingShingle	Biology (General) QH301-705.5 Anna K. Uryga Mandy O. J. Grootaert Abel M. Garrido Sebnem Oc Kirsty Foote Joel Chappell Alison Finigan Francesca Rossiello Fabrizio d’Adda di Fagagna Dimitra Aravani Helle F. Jorgensen Martin R. Bennett Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury
description	Anna Uryga and Mandy Grootaert et al. combine cell culture and animal models to examine how senescence of human vascular smooth muscle cells (VSMCs) and persistent telomere damage drive inflammation. Their results suggest that telomere injury can be the primary cause of premature senescence in VSMCs, and that DNA damage can be a major cause of persistent inflammation in vascular disease.
format	article
author	Anna K. Uryga Mandy O. J. Grootaert Abel M. Garrido Sebnem Oc Kirsty Foote Joel Chappell Alison Finigan Francesca Rossiello Fabrizio d’Adda di Fagagna Dimitra Aravani Helle F. Jorgensen Martin R. Bennett
author_facet	Anna K. Uryga Mandy O. J. Grootaert Abel M. Garrido Sebnem Oc Kirsty Foote Joel Chappell Alison Finigan Francesca Rossiello Fabrizio d’Adda di Fagagna Dimitra Aravani Helle F. Jorgensen Martin R. Bennett
author_sort	Anna K. Uryga
title	Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury
title_short	Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury
title_full	Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury
title_fullStr	Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury
title_full_unstemmed	Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury
title_sort	telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury
publisher	Nature Portfolio
publishDate	2021
url	https://doaj.org/article/89fb7bb2970a4e30ac925d9236fd3bc3
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Telomere damage promotes vascular smooth muscle cell senescence and immune cell recruitment after vessel injury

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