Diet induces hepatocyte protection in fatty liver disease via modulation of PTEN signaling.
PTEN
alcoholic liver disease
alcoholic steatohepatitis
cell signaling
fatty liver
non-alcoholic fatty liver disease
non-alcoholic steatohepatitis
reactive oxygen species
Journal
Biomedical reports
ISSN: 2049-9434
Titre abrégé: Biomed Rep
Pays: England
ID NLM: 101613227
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
received:
10
04
2019
accepted:
11
07
2019
entrez:
9
5
2020
pubmed:
10
5
2020
medline:
10
5
2020
Statut:
ppublish
Résumé
Fatty liver disease (FLD) is characterized by accumulation of excess fat in the liver. The underlying molecular mechanism associated with the progression of the disease has been in elusive. Hepatocellular demise due to increased oxidative stress resulting in an inflammatory response may be a key feature in FLD. Recent advances in molecular biology have led to an improved understanding of the molecular pathogenesis, suggesting a critical association between the PI3K/AKT/PTEN signaling pathway and FLD. In particular, PTEN has been associated with regulating the pathogenesis of hepatocyte degeneration. Given the function of mitochondria in reactive oxygen species (ROS) generation and the initiation of oxidative stress, the mitochondrial antioxidant network is of interest. It is vital to balance the activity of intracellular key molecules to maintain a healthy liver. Consequently, onset of FLD may be delayed using dietary protective agents that alter PTEN signaling and reduce ROS levels. The advancement of research on dietary regulation with a focus on modulatory roles in ROS generation and PTEN associated signaling is summarized in the current study, supporting further preventive and therapeutic exploration.
Identifiants
pubmed: 32382414
doi: 10.3892/br.2020.1299
pii: BR-0-0-1299
pmc: PMC7201141
doi:
Types de publication
Journal Article
Langues
eng
Pagination
295-302Informations de copyright
Copyright: © Ikeda et al.
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