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The essential effect of mTORC1-dependent lipophagy in non-alcoholic fatty liver disease

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FRONTIERS IN PHARMACOLOGY
卷 14, 期 -, 页码 -

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FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2023.1124003

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NAFLD; lipophagy; mTORC1; hepatic steatosis; insulin resistance; hepatic fibrosis

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Non-alcoholic fatty liver disease (NAFLD) is a chronic progressive liver disease with increasing prevalence. Abnormal regulation of lipophagy in NAFLD patients indicates the potential role of mTORC1 in restoring failed autophagy. Targeting mTORC1 to promote lipophagy has the potential to become an effective therapeutic strategy for NAFLD. This article provides an overview of the main pathways through which mTORC1 participates in lipophagy formation and the intervention effect of mTORC1-regulated lipophagy in NAFLD, offering new therapeutic strategies for the prevention and treatment of NAFLD in the future.
Non-alcoholic fatty liver disease (NAFLD) is a chronic progressive liver disease with increasing prevalence. Lipophagy is a type of programmed cell death that plays an essential role in maintaining the body's balance of fatty acid metabolism. However, the livers of NAFLD patients are abnormally dysregulated in lipophagy. mTORC1 is a critical negative regulator of lipophagy, which has been confirmed to participate in the process of lipophagy through various complex mechanisms. Therefore, targeting mTORC1 to restore failed autophagy may be an effective therapeutic strategy for NAFLD. This article reviews the main pathways through which mTORC1 participates in the formation of lipophagy and the intervention effect of mTORC1-regulated lipophagy in NAFLD, providing new therapeutic strategies for the prevention and treatment of NAFLD in the future.

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