PMID- 38001781
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20231128
IS  - 2076-3921 (Print)
IS  - 2076-3921 (Electronic)
IS  - 2076-3921 (Linking)
VI  - 12
IP  - 11
DP  - 2023 Oct 29
TI  - The Roles of NFR2-Regulated Oxidative Stress and Mitochondrial Quality Control in 
      Chronic Liver Diseases.
LID - 10.3390/antiox12111928 [doi]
LID - 1928
AB  - Chronic liver disease (CLD) affects a significant portion of the global 
      population, leading to a substantial number of deaths each year. Distinct forms 
      like non-alcoholic fatty liver disease (NAFLD) and alcoholic fatty liver disease 
      (ALD), though they have different etiologies, highlight shared pathologies rooted 
      in oxidative stress. Central to liver metabolism, mitochondria are essential for 
      ATP production, gluconeogenesis, fatty acid oxidation, and heme synthesis. 
      However, in diseases like NAFLD, ALD, and liver fibrosis, mitochondrial function 
      is compromised by inflammatory cytokines, hepatotoxins, and metabolic 
      irregularities. This dysfunction, especially electron leakage, exacerbates the 
      production of reactive oxygen species (ROS), augmenting liver damage. Amidst 
      this, nuclear factor erythroid 2-related factor 2 (NRF2) emerges as a cellular 
      protector. It not only counters oxidative stress by regulating antioxidant genes 
      but also maintains mitochondrial health by overseeing autophagy and biogenesis. 
      The synergy between NRF2 modulation and mitochondrial function introduces new 
      therapeutic potentials for CLD, focusing on preserving mitochondrial integrity 
      against oxidative threats. This review delves into the intricate role of 
      oxidative stress in CLD, shedding light on innovative strategies for its 
      prevention and treatment, especially through the modulation of the NRF2 and 
      mitochondrial pathways.
FAU - Park, Jeong-Su
AU  - Park JS
AUID- ORCID: 0000-0002-3667-9970
AD  - College of Pharmacy and Medical Research Center, Chungbuk National University, 
      Cheongju 28160, Republic of Korea.
FAU - Rustamov, Nodir
AU  - Rustamov N
AUID- ORCID: 0000-0003-3691-4974
AD  - College of Pharmacy and Medical Research Center, Chungbuk National University, 
      Cheongju 28160, Republic of Korea.
FAU - Roh, Yoon-Seok
AU  - Roh YS
AD  - College of Pharmacy and Medical Research Center, Chungbuk National University, 
      Cheongju 28160, Republic of Korea.
LA  - eng
GR  - 2017R1A5A2015541/National Research Foundation of Korea/
GR  - 20182MFDS425/Korean Food and Drug Administration/
GR  - 2021RIS-001/Regional Innovation Strategy (RIS) of the National Research 
      Foundation of Korea/
PT  - Journal Article
PT  - Review
DEP - 20231029
PL  - Switzerland
TA  - Antioxidants (Basel)
JT  - Antioxidants (Basel, Switzerland)
JID - 101668981
PMC - PMC10669501
OTO - NOTNLM
OT  - CLD
OT  - NRF2
OT  - ROS
OT  - antioxidants
OT  - mitochondria
OT  - oxidative stress
COIS- The authors declare no conflict of interest.
EDAT- 2023/11/25 12:46
MHDA- 2023/11/25 12:47
PMCR- 2023/10/29
CRDT- 2023/11/25 01:06
PHST- 2023/09/28 00:00 [received]
PHST- 2023/10/24 00:00 [revised]
PHST- 2023/10/27 00:00 [accepted]
PHST- 2023/11/25 12:47 [medline]
PHST- 2023/11/25 12:46 [pubmed]
PHST- 2023/11/25 01:06 [entrez]
PHST- 2023/10/29 00:00 [pmc-release]
AID - antiox12111928 [pii]
AID - antioxidants-12-01928 [pii]
AID - 10.3390/antiox12111928 [doi]
PST - epublish
SO  - Antioxidants (Basel). 2023 Oct 29;12(11):1928. doi: 10.3390/antiox12111928.