The Role of Notch Signaling Pathway in Non-Alcoholic Fatty Liver Disease

Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide, and progressive NAFLD can develop into non-alcoholic steatohepatitis (NASH), liver cirrhosis, or hepatocellular carcinoma (HCC). NAFLD is a kind of metabolic disordered disease, which is commonly associated...

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Autores principales:	Hao Xu, Lin Wang
Formato:	article
Lenguaje:	EN
Publicado:	Frontiers Media S.A. 2021
Materias:	Notch signaling pathway non-alcoholic fatty liver disease (NAFLD) steatohepatitis lipid metabolism insulin resistance (IR) fibrogenesis Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/2024b89b411a42caa3e134689ed0005b
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spelling	oai:doaj.org-article:2024b89b411a42caa3e134689ed0005b2021-11-30T18:38:41ZThe Role of Notch Signaling Pathway in Non-Alcoholic Fatty Liver Disease2296-889X10.3389/fmolb.2021.792667https://doaj.org/article/2024b89b411a42caa3e134689ed0005b2021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fmolb.2021.792667/fullhttps://doaj.org/toc/2296-889XNon-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide, and progressive NAFLD can develop into non-alcoholic steatohepatitis (NASH), liver cirrhosis, or hepatocellular carcinoma (HCC). NAFLD is a kind of metabolic disordered disease, which is commonly associated with lipid metabolism, insulin resistance, oxidative stress, inflammation, and fibrogenesis, as well as autophagy. Growing studies have shown Notch signaling pathway plays a pivotal role in the regulation of NAFLD progression. Here, we review the profile of the Notch signaling pathway, new evidence of Notch signaling involvement in NAFLD, and describe the potential of Notch as a biomarker and therapeutic target for NAFLD treatment.Hao XuLin WangFrontiers Media S.A.articleNotch signaling pathwaynon-alcoholic fatty liver disease (NAFLD)steatohepatitislipid metabolisminsulin resistance (IR)fibrogenesisBiology (General)QH301-705.5ENFrontiers in Molecular Biosciences, Vol 8 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Notch signaling pathway non-alcoholic fatty liver disease (NAFLD) steatohepatitis lipid metabolism insulin resistance (IR) fibrogenesis Biology (General) QH301-705.5
spellingShingle	Notch signaling pathway non-alcoholic fatty liver disease (NAFLD) steatohepatitis lipid metabolism insulin resistance (IR) fibrogenesis Biology (General) QH301-705.5 Hao Xu Lin Wang The Role of Notch Signaling Pathway in Non-Alcoholic Fatty Liver Disease
description	Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide, and progressive NAFLD can develop into non-alcoholic steatohepatitis (NASH), liver cirrhosis, or hepatocellular carcinoma (HCC). NAFLD is a kind of metabolic disordered disease, which is commonly associated with lipid metabolism, insulin resistance, oxidative stress, inflammation, and fibrogenesis, as well as autophagy. Growing studies have shown Notch signaling pathway plays a pivotal role in the regulation of NAFLD progression. Here, we review the profile of the Notch signaling pathway, new evidence of Notch signaling involvement in NAFLD, and describe the potential of Notch as a biomarker and therapeutic target for NAFLD treatment.
format	article
author	Hao Xu Lin Wang
author_facet	Hao Xu Lin Wang
author_sort	Hao Xu
title	The Role of Notch Signaling Pathway in Non-Alcoholic Fatty Liver Disease
title_short	The Role of Notch Signaling Pathway in Non-Alcoholic Fatty Liver Disease
title_full	The Role of Notch Signaling Pathway in Non-Alcoholic Fatty Liver Disease
title_fullStr	The Role of Notch Signaling Pathway in Non-Alcoholic Fatty Liver Disease
title_full_unstemmed	The Role of Notch Signaling Pathway in Non-Alcoholic Fatty Liver Disease
title_sort	role of notch signaling pathway in non-alcoholic fatty liver disease
publisher	Frontiers Media S.A.
publishDate	2021
url	https://doaj.org/article/2024b89b411a42caa3e134689ed0005b
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The Role of Notch Signaling Pathway in Non-Alcoholic Fatty Liver Disease

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