PMID- 36632321
OWN - NLM
STAT- MEDLINE
DCOM- 20230215
LR  - 20230215
IS  - 2219-2840 (Electronic)
IS  - 1007-9327 (Print)
IS  - 1007-9327 (Linking)
VI  - 28
IP  - 48
DP  - 2022 Dec 28
TI  - Nuclear factor erythroid 2-related factor 2-mediated signaling and metabolic 
      associated fatty liver disease.
PG  - 6909-6921
LID - 10.3748/wjg.v28.i48.6909 [doi]
AB  - Oxidative stress is a key driver in the development and progression of several 
      diseases, including metabolic associated fatty liver disease (MAFLD). This 
      condition includes a wide spectrum of pathological injuries, extending from 
      simple steatosis to inflammation, fibrosis, cirrhosis, and hepatocellular 
      carcinoma. Excessive buildup of lipids in the liver is strictly related to 
      oxidative stress in MAFLD, progressing to liver fibrosis and cirrhosis. The 
      nuclear factor erythroid 2-related factor 2 (NRF2) is a master regulator of redox 
      homeostasis. NRF2 plays an important role for cellular protection by inducing the 
      expression of genes related to antioxidant, anti-inflammatory, and cytoprotective 
      response. Consistent evidence demonstrates that NRF2 is involved in every step of 
      MAFLD deve-lopment, from simple steatosis to inflammation, advanced fibrosis, and 
      ini-tiation/progression of hepatocellular carcinoma. NRF2 activators regulate 
      lipid metabolism and oxidative stress alleviating the fatty liver disease by 
      inducing the expression of cytoprotective genes. Thus, modulating NRF2 activation 
      is crucial not only in understanding specific mechanisms underlying MAFLD 
      progression but also to characterize effective therapeutic strategies. This 
      review outlined the current knowledge on the effects of NRF2 pathway, modulators, 
      and mechanisms involved in the therapeutic implications of liver steatosis, 
      inflammation, and fibrosis in MAFLD.
CI  - (c)The Author(s) 2022. Published by Baishideng Publishing Group Inc. All rights 
      reserved.
FAU - Bukke, Vidyasagar Naik
AU  - Bukke VN
AD  - Department of Medical and Surgical Sciences, University of Foggia, Foggia 71122, 
      Italy.
FAU - Moola, Archana
AU  - Moola A
AD  - Department of Medical and Surgical Sciences, University of Foggia, Foggia 71122, 
      Italy.
FAU - Serviddio, Gaetano
AU  - Serviddio G
AD  - Department of Medical and Surgical Sciences, University of Foggia, Foggia 71122, 
      Italy.
FAU - Vendemiale, Gianluigi
AU  - Vendemiale G
AD  - Department of Medical and Surgical Sciences, University of Foggia, Foggia 71122, 
      Italy.
FAU - Bellanti, Francesco
AU  - Bellanti F
AD  - Department of Medical and Surgical Sciences, University of Foggia, Foggia 71122, 
      Italy. francesco.bellanti@unifg.it.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - World J Gastroenterol
JT  - World journal of gastroenterology
JID - 100883448
RN  - 0 (NF-E2-Related Factor 2)
SB  - IM
MH  - Humans
MH  - Carcinoma, Hepatocellular/metabolism
MH  - Liver/metabolism/pathology
MH  - Liver Cirrhosis/metabolism
MH  - Liver Neoplasms/metabolism
MH  - *NF-E2-Related Factor 2/metabolism
MH  - *Non-alcoholic Fatty Liver Disease/metabolism
MH  - *Oxidative Stress
PMC - PMC9827579
OTO - NOTNLM
OT  - Antioxidants
OT  - Liver injury
OT  - Metabolic-associated fatty liver disease
OT  - Nonalcoholic fatty liver disease
OT  - Nuclear factor erythroid 2-related factor 2
OT  - Oxidative stress
COIS- Conflict-of-interest statement: All authors declare no conflicts of interests for 
      this article.
EDAT- 2023/01/13 06:00
MHDA- 2023/01/14 06:00
PMCR- 2022/12/28
CRDT- 2023/01/12 01:58
PHST- 2022/09/18 00:00 [received]
PHST- 2022/11/05 00:00 [revised]
PHST- 2022/11/22 00:00 [accepted]
PHST- 2023/01/12 01:58 [entrez]
PHST- 2023/01/13 06:00 [pubmed]
PHST- 2023/01/14 06:00 [medline]
PHST- 2022/12/28 00:00 [pmc-release]
AID - 10.3748/wjg.v28.i48.6909 [doi]
PST - ppublish
SO  - World J Gastroenterol. 2022 Dec 28;28(48):6909-6921. doi: 
      10.3748/wjg.v28.i48.6909.