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The cGAS–STING signaling in cardiovascular and metabolic diseases: Future novel target option for pharmacotherapy
The cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING) signaling exert essential regulatory function in microbial-and onco-immunology through the induction of cytokines, primarily type I interferons. Recently, the aberrant and deranged signaling of the cGAS–STING axis is closely i...
Autores principales: | , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799861/ https://www.ncbi.nlm.nih.gov/pubmed/35127372 http://dx.doi.org/10.1016/j.apsb.2021.05.011 |
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author | Oduro, Patrick Kwabena Zheng, Xianxian Wei, Jinna Yang, Yanze Wang, Yuefei Zhang, Han Liu, Erwei Gao, Xiumei Du, Mei Wang, Qilong |
author_facet | Oduro, Patrick Kwabena Zheng, Xianxian Wei, Jinna Yang, Yanze Wang, Yuefei Zhang, Han Liu, Erwei Gao, Xiumei Du, Mei Wang, Qilong |
author_sort | Oduro, Patrick Kwabena |
collection | PubMed |
description | The cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING) signaling exert essential regulatory function in microbial-and onco-immunology through the induction of cytokines, primarily type I interferons. Recently, the aberrant and deranged signaling of the cGAS–STING axis is closely implicated in multiple sterile inflammatory diseases, including heart failure, myocardial infarction, cardiac hypertrophy, nonalcoholic fatty liver diseases, aortic aneurysm and dissection, obesity, etc. This is because of the massive loads of damage-associated molecular patterns (mitochondrial DNA, DNA in extracellular vesicles) liberated from recurrent injury to metabolic cellular organelles and tissues, which are sensed by the pathway. Also, the cGAS–STING pathway crosstalk with essential intracellular homeostasis processes like apoptosis, autophagy, and regulate cellular metabolism. Targeting derailed STING signaling has become necessary for chronic inflammatory diseases. Meanwhile, excessive type I interferons signaling impact on cardiovascular and metabolic health remain entirely elusive. In this review, we summarize the intimate connection between the cGAS–STING pathway and cardiovascular and metabolic disorders. We also discuss some potential small molecule inhibitors for the pathway. This review provides insight to stimulate interest in and support future research into understanding this signaling axis in cardiovascular and metabolic tissues and diseases. |
format | Online Article Text |
id | pubmed-8799861 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Elsevier |
record_format | MEDLINE/PubMed |
spelling | pubmed-87998612022-02-03 The cGAS–STING signaling in cardiovascular and metabolic diseases: Future novel target option for pharmacotherapy Oduro, Patrick Kwabena Zheng, Xianxian Wei, Jinna Yang, Yanze Wang, Yuefei Zhang, Han Liu, Erwei Gao, Xiumei Du, Mei Wang, Qilong Acta Pharm Sin B Review The cyclic GMP–AMP synthase (cGAS)–stimulator of interferon genes (STING) signaling exert essential regulatory function in microbial-and onco-immunology through the induction of cytokines, primarily type I interferons. Recently, the aberrant and deranged signaling of the cGAS–STING axis is closely implicated in multiple sterile inflammatory diseases, including heart failure, myocardial infarction, cardiac hypertrophy, nonalcoholic fatty liver diseases, aortic aneurysm and dissection, obesity, etc. This is because of the massive loads of damage-associated molecular patterns (mitochondrial DNA, DNA in extracellular vesicles) liberated from recurrent injury to metabolic cellular organelles and tissues, which are sensed by the pathway. Also, the cGAS–STING pathway crosstalk with essential intracellular homeostasis processes like apoptosis, autophagy, and regulate cellular metabolism. Targeting derailed STING signaling has become necessary for chronic inflammatory diseases. Meanwhile, excessive type I interferons signaling impact on cardiovascular and metabolic health remain entirely elusive. In this review, we summarize the intimate connection between the cGAS–STING pathway and cardiovascular and metabolic disorders. We also discuss some potential small molecule inhibitors for the pathway. This review provides insight to stimulate interest in and support future research into understanding this signaling axis in cardiovascular and metabolic tissues and diseases. Elsevier 2022-01 2021-05-20 /pmc/articles/PMC8799861/ /pubmed/35127372 http://dx.doi.org/10.1016/j.apsb.2021.05.011 Text en © 2022 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/). |
spellingShingle | Review Oduro, Patrick Kwabena Zheng, Xianxian Wei, Jinna Yang, Yanze Wang, Yuefei Zhang, Han Liu, Erwei Gao, Xiumei Du, Mei Wang, Qilong The cGAS–STING signaling in cardiovascular and metabolic diseases: Future novel target option for pharmacotherapy |
title | The cGAS–STING signaling in cardiovascular and metabolic diseases: Future novel target option for pharmacotherapy |
title_full | The cGAS–STING signaling in cardiovascular and metabolic diseases: Future novel target option for pharmacotherapy |
title_fullStr | The cGAS–STING signaling in cardiovascular and metabolic diseases: Future novel target option for pharmacotherapy |
title_full_unstemmed | The cGAS–STING signaling in cardiovascular and metabolic diseases: Future novel target option for pharmacotherapy |
title_short | The cGAS–STING signaling in cardiovascular and metabolic diseases: Future novel target option for pharmacotherapy |
title_sort | cgas–sting signaling in cardiovascular and metabolic diseases: future novel target option for pharmacotherapy |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8799861/ https://www.ncbi.nlm.nih.gov/pubmed/35127372 http://dx.doi.org/10.1016/j.apsb.2021.05.011 |
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