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...
| Main Authors: | , , , |
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2023-03-01
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| Series: | Frontiers in Nutrition |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fnut.2023.1139339/full |
| _version_ | 1811162617793740800 |
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| author | Honggui Li Xinlei Guo Eduardo Aquino Chaodong Wu |
| author_facet | Honggui Li Xinlei Guo Eduardo Aquino Chaodong Wu |
| author_sort | Honggui Li |
| collection | DOAJ |
| 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. |
| first_indexed | 2024-04-10T06:32:16Z |
| format | Article |
| id | doaj.art-c873f605aa2845bea2563fd5d5aa4baa |
| institution | Directory Open Access Journal |
| issn | 2296-861X |
| language | English |
| last_indexed | 2024-04-10T06:32:16Z |
| publishDate | 2023-03-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Nutrition |
| spelling | doaj.art-c873f605aa2845bea2563fd5d5aa4baa2023-03-01T06:50:52ZengFrontiers Media S.A.Frontiers in Nutrition2296-861X2023-03-011010.3389/fnut.2023.11393391139339Mini review: STING activation during non-alcoholic fatty liver diseaseHonggui LiXinlei GuoEduardo AquinoChaodong WuNon-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.https://www.frontiersin.org/articles/10.3389/fnut.2023.1139339/fullnon-alcoholic fatty liver diseaseliver fibrosisinflammationstimulator of interferon genesmacrophage |
| spellingShingle | Honggui Li Xinlei Guo Eduardo Aquino Chaodong Wu Mini review: STING activation during non-alcoholic fatty liver disease Frontiers in Nutrition non-alcoholic fatty liver disease liver fibrosis inflammation stimulator of interferon genes macrophage |
| 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 | non-alcoholic fatty liver disease liver fibrosis inflammation stimulator of interferon genes macrophage |
| url | https://www.frontiersin.org/articles/10.3389/fnut.2023.1139339/full |
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