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Mini review: STING activation during non-alcoholic fatty liver disease
Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic diseases serving as a major threat to human health. While the pathogenesis of NAFLD is multi-factorial, inflammation is considered a critical factor driving the development and progression of NAFLD phenotype, including liver...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2023
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10014842/ https://www.ncbi.nlm.nih.gov/pubmed/36937350 http://dx.doi.org/10.3389/fnut.2023.1139339 |
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author | Li, Honggui Guo, Xinlei Aquino, Eduardo Wu, Chaodong |
author_facet | Li, Honggui Guo, Xinlei Aquino, Eduardo Wu, Chaodong |
author_sort | Li, Honggui |
collection | PubMed |
description | Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic diseases serving as a major threat to human health. While the pathogenesis of NAFLD is multi-factorial, inflammation is considered a critical factor driving the development and progression of NAFLD phenotype, including liver fibrosis. As an essential mediator of innate immunity, stimulator of interferon genes (STING) functions to promote anti-viral immunity. Accumulating evidence also indicates that STING functions to promote the proinflammatory activation of several types of liver cells, especially macrophages/Kupffer cells, in a manner independent of interferon production. Over the past several years, a significant body of literature has validated a detrimental role for STING in regulating the pathogenesis of hepatic steatosis and inflammation. In particular, the STING in macrophages/Kupffer cells has attracted much attention due to its importance in not only enhancing macrophage proinflammatory activation, but also generating macrophage-derived mediators to increase hepatocyte fat deposition and proinflammatory responses, and to activate hepatic stellate cell fibrogenic activation. Both intracellular and extracellular signals are participating in STING activation in macrophages, thereby critically contributing to NAFLD phenotype. This mini review summarizes recent advances on how STING is activated in macrophages in the context of NAFLD pathophysiology. |
format | Online Article Text |
id | pubmed-10014842 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-100148422023-03-16 Mini review: STING activation during non-alcoholic fatty liver disease Li, Honggui Guo, Xinlei Aquino, Eduardo Wu, Chaodong Front Nutr Nutrition Non-alcoholic fatty liver disease (NAFLD) is one of the most common chronic diseases serving as a major threat to human health. While the pathogenesis of NAFLD is multi-factorial, inflammation is considered a critical factor driving the development and progression of NAFLD phenotype, including liver fibrosis. As an essential mediator of innate immunity, stimulator of interferon genes (STING) functions to promote anti-viral immunity. Accumulating evidence also indicates that STING functions to promote the proinflammatory activation of several types of liver cells, especially macrophages/Kupffer cells, in a manner independent of interferon production. Over the past several years, a significant body of literature has validated a detrimental role for STING in regulating the pathogenesis of hepatic steatosis and inflammation. In particular, the STING in macrophages/Kupffer cells has attracted much attention due to its importance in not only enhancing macrophage proinflammatory activation, but also generating macrophage-derived mediators to increase hepatocyte fat deposition and proinflammatory responses, and to activate hepatic stellate cell fibrogenic activation. Both intracellular and extracellular signals are participating in STING activation in macrophages, thereby critically contributing to NAFLD phenotype. This mini review summarizes recent advances on how STING is activated in macrophages in the context of NAFLD pathophysiology. Frontiers Media S.A. 2023-03-01 /pmc/articles/PMC10014842/ /pubmed/36937350 http://dx.doi.org/10.3389/fnut.2023.1139339 Text en Copyright © 2023 Li, Guo, Aquino and Wu. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Nutrition Li, Honggui Guo, Xinlei Aquino, Eduardo Wu, Chaodong Mini review: STING activation during non-alcoholic fatty liver disease |
title | Mini review: STING activation during non-alcoholic fatty liver disease |
title_full | Mini review: STING activation during non-alcoholic fatty liver disease |
title_fullStr | Mini review: STING activation during non-alcoholic fatty liver disease |
title_full_unstemmed | Mini review: STING activation during non-alcoholic fatty liver disease |
title_short | Mini review: STING activation during non-alcoholic fatty liver disease |
title_sort | mini review: sting activation during non-alcoholic fatty liver disease |
topic | Nutrition |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10014842/ https://www.ncbi.nlm.nih.gov/pubmed/36937350 http://dx.doi.org/10.3389/fnut.2023.1139339 |
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