Impact of Glucoraphanin-Mediated Activation of Nrf2 on Non-Alcoholic Fatty Liver Disease with a Focus on Mitochondrial Dysfunction.


Journal

International journal of molecular sciences
ISSN: 1422-0067
Titre abrégé: Int J Mol Sci
Pays: Switzerland
ID NLM: 101092791

Informations de publication

Date de publication:
25 Nov 2019
Historique:
received: 31 10 2019
revised: 19 11 2019
accepted: 23 11 2019
entrez: 29 11 2019
pubmed: 30 11 2019
medline: 6 5 2020
Statut: epublish

Résumé

Non-alcoholic fatty liver disease (NAFLD) is a common disease in Western nations and ranges in severity from steatosis to steatohepatitis (NASH). NAFLD is a genetic-environmental-metabolic stress-related disease of unclear pathogenesis. NAFLD is triggered by caloric overconsumption and physical inactivity, which lead to insulin resistance and oxidative stress. A growing body of evidence indicates that mitochondrial dysfunction plays a critical role in the pathogenesis of NAFLD. Mitochondrial dysfunction not only promotes fat accumulation, but also leads to generation of reactive oxygen species (ROS) and lipid peroxidation, resulting in oxidative stress in hepatocytes. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important modulator of antioxidant signaling that serves as a primary cellular defense against the cytotoxic effects of oxidative stress. The pharmacological induction of Nrf2 ameliorates obesity-associated insulin resistance and NAFLD in a mouse model. Sulforaphane and its precursor glucoraphanin are derived from broccoli sprouts and are the most potent natural Nrf2 inducers-they may protect mitochondrial function, thus suppressing the development of NASH. In this review, we briefly describe the role of mitochondrial dysfunction in the pathogenesis of NASH and the effects of glucoraphanin on its development.

Identifiants

pubmed: 31775341
pii: ijms20235920
doi: 10.3390/ijms20235920
pmc: PMC6929181
pii:
doi:

Substances chimiques

Glucosinolates 0
Imidoesters 0
NF-E2-Related Factor 2 0
Oximes 0
Sulfoxides 0
glucoraphanin Q86A197713

Types de publication

Journal Article Review

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : Japan Society for the Promotion of Science KAKENHI (T.O.)
ID : 15K12698, 16H03035
Organisme : Japan Society for the Promotion of Science KAKENHI (N.N.)
ID : 15K00813

Déclaration de conflit d'intérêts

The authors declare no conflict of interest.

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Auteurs

Liang Xu (L)

Key Laboratory of Laboratory Medicine, School of Laboratory Medicine and Life Science, Wenzhou Medical University, Wenzhou 325035, China.
Department of Cell Metabolism and Nutrition, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan.

Naoto Nagata (N)

Department of Cell Metabolism and Nutrition, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan.

Tsuguhito Ota (T)

Department of Cell Metabolism and Nutrition, Advanced Preventive Medical Sciences Research Center, Kanazawa University, Kanazawa, Ishikawa 920-8640, Japan.
Division of Metabolism and Biosystemic Science, Department of Medicine, Asahikawa Medical University, Asahikawa, Hokkaido 078-8510, Japan.

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