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The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities

BACKGROUND: The global population of older individuals is growing, and ageing is a key risk factor for atherosclerotic cardiovascular diseases. Abnormal accumulation of senescent cells can cause potentially deleterious effects on the organism with age. As a vital marker of cellular senescence, the s...

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Autores principales: Sun, Yu, Wang, Xia, Liu, Tianwei, Zhu, Xiaoyan, Pan, Xudong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9153125/
https://www.ncbi.nlm.nih.gov/pubmed/35642067
http://dx.doi.org/10.1186/s13578-022-00815-5
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author Sun, Yu
Wang, Xia
Liu, Tianwei
Zhu, Xiaoyan
Pan, Xudong
author_facet Sun, Yu
Wang, Xia
Liu, Tianwei
Zhu, Xiaoyan
Pan, Xudong
author_sort Sun, Yu
collection PubMed
description BACKGROUND: The global population of older individuals is growing, and ageing is a key risk factor for atherosclerotic cardiovascular diseases. Abnormal accumulation of senescent cells can cause potentially deleterious effects on the organism with age. As a vital marker of cellular senescence, the senescence-associated secretory phenotype (SASP) is a novel mechanism to link cellular senescence with atherosclerosis. MAIN BODY: In this review, we concretely describe the characteristics of the SASP and its regulation mechanisms. Importantly, we provide novel perspectives on how the SASP can promote atherosclerosis. The SASP from different types of senescent cells have vital roles in atherosclerosis progression. As a significant mediator of the harmful effects of senescent cells, it can play a pro-atherogenic role by producing inflammation and immune dysfunction. Furthermore, the SASP can deliver senescence signals to the surrounding vascular cells, gradually contributing to the development of atherosclerosis. Finally, we focus on a variety of novel therapeutic strategies aimed to reduce the burden of atherosclerosis in elderly individuals by targeting senescent cells and inhibiting the regulatory mechanisms of the SASP. CONCLUSION: This review systematically summarizes the multiple roles of the SASP in atherosclerosis and can contribute to the exploration of new therapeutic opportunities.
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spelling pubmed-91531252022-06-01 The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities Sun, Yu Wang, Xia Liu, Tianwei Zhu, Xiaoyan Pan, Xudong Cell Biosci Review BACKGROUND: The global population of older individuals is growing, and ageing is a key risk factor for atherosclerotic cardiovascular diseases. Abnormal accumulation of senescent cells can cause potentially deleterious effects on the organism with age. As a vital marker of cellular senescence, the senescence-associated secretory phenotype (SASP) is a novel mechanism to link cellular senescence with atherosclerosis. MAIN BODY: In this review, we concretely describe the characteristics of the SASP and its regulation mechanisms. Importantly, we provide novel perspectives on how the SASP can promote atherosclerosis. The SASP from different types of senescent cells have vital roles in atherosclerosis progression. As a significant mediator of the harmful effects of senescent cells, it can play a pro-atherogenic role by producing inflammation and immune dysfunction. Furthermore, the SASP can deliver senescence signals to the surrounding vascular cells, gradually contributing to the development of atherosclerosis. Finally, we focus on a variety of novel therapeutic strategies aimed to reduce the burden of atherosclerosis in elderly individuals by targeting senescent cells and inhibiting the regulatory mechanisms of the SASP. CONCLUSION: This review systematically summarizes the multiple roles of the SASP in atherosclerosis and can contribute to the exploration of new therapeutic opportunities. BioMed Central 2022-05-31 /pmc/articles/PMC9153125/ /pubmed/35642067 http://dx.doi.org/10.1186/s13578-022-00815-5 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Review
Sun, Yu
Wang, Xia
Liu, Tianwei
Zhu, Xiaoyan
Pan, Xudong
The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities
title The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities
title_full The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities
title_fullStr The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities
title_full_unstemmed The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities
title_short The multifaceted role of the SASP in atherosclerosis: from mechanisms to therapeutic opportunities
title_sort multifaceted role of the sasp in atherosclerosis: from mechanisms to therapeutic opportunities
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9153125/
https://www.ncbi.nlm.nih.gov/pubmed/35642067
http://dx.doi.org/10.1186/s13578-022-00815-5
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