PMID- 35222075
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220301
IS  - 1664-042X (Print)
IS  - 1664-042X (Electronic)
IS  - 1664-042X (Linking)
VI  - 13
DP  - 2022
TI  - MicroRNA-122-5p Inhibition Improves Inflammation and Oxidative Stress Damage in 
      Dietary-Induced Non-alcoholic Fatty Liver Disease Through Targeting FOXO3.
PG  - 803445
LID - 10.3389/fphys.2022.803445 [doi]
LID - 803445
AB  - Misregulated microRNA network has been emerging as the main regulator in 
      non-alcoholic fatty liver disease (NAFLD). The deregulation of miR-122-5p is 
      associated with the liver disease. However, the specific role and molecular 
      mechanism of miR-122-5p in NAFLD remain unclear. In this study, we have reported 
      that the high-fat diet (HFD) or palmitic acid (PA) significantly upregulated the 
      hepatic miR-122-5p expression in vivo and in vitro. Inhibition of miR-122-5p 
      suppressed accumulation-induced inflammation of lipids and oxidative stress 
      damage in PA-treated L02 cells and HFD-induced fatty liver. The effect of the 
      miR-122-5p inhibitor on NAFLD did not depend on insulin resistance-mediated 
      PI3K/AKT/mammalian target of rapamycin (mTOR) signaling pathway but rather on the 
      upregulation of its downstream FOXO3. Subsequently, we validated that miR-122-5p 
      directly binds to the predicted 3'-UTR of FOXO3 to inhibit its gene expression. 
      Conversely, silencing FOXO3 abolished the hepatic benefits of miR-122-5p 
      inhibition to obese mice by decreasing the activity of antioxidant enzymes of 
      superoxide dismutase (SOD). This study provides a novel finding that FOXO3 was 
      the target gene of miR-122-5p to attenuate inflammatory response and oxidative 
      stress damage in dietary-induced NAFLD. Our study provided evidence to reveal the 
      physiological role of miR-122-5p in dietary-induced NAFLD.
CI  - Copyright (c) 2022 Hu, Peng, Du, Zhang, Zhai, Xiong and Luo.
FAU - Hu, Yiyi
AU  - Hu Y
AD  - Department of Gestroenterology, Shunde Hospital of Southern Medical University, 
      Foshan, China.
AD  - Department of VIP Medical Center, Shunde Hospital of Southern Medical University, 
      Foshan, China.
FAU - Peng, Xuetao
AU  - Peng X
AD  - Department of Gestroenterology, Shunde Hospital of Southern Medical University, 
      Foshan, China.
FAU - Du, Guoping
AU  - Du G
AD  - Department of Gestroenterology, Shunde Hospital of Southern Medical University, 
      Foshan, China.
FAU - Zhang, Zhiqiao
AU  - Zhang Z
AD  - Department of Infectious Diseases, Shunde Hospital of Southern Medical 
      University, Foshan, China.
FAU - Zhai, Yingji
AU  - Zhai Y
AD  - Department of Gestroenterology, Shunde Hospital of Southern Medical University, 
      Foshan, China.
FAU - Xiong, Xingbo
AU  - Xiong X
AD  - Department of Gestroenterology, Shunde Hospital of Southern Medical University, 
      Foshan, China.
FAU - Luo, Xiaoliang
AU  - Luo X
AD  - Department of Gestroenterology, Shunde Hospital of Southern Medical University, 
      Foshan, China.
LA  - eng
PT  - Journal Article
DEP - 20220211
PL  - Switzerland
TA  - Front Physiol
JT  - Frontiers in physiology
JID - 101549006
PMC - PMC8874326
OTO - NOTNLM
OT  - FOXO3
OT  - inflammation
OT  - miR-122-5p
OT  - non-alcoholic fatty liver disease
OT  - oxidative stress
COIS- The authors declare that the research was conducted in the absence of any 
      commercial or financial relationships that could be construed as a potential 
      conflict of interest.
EDAT- 2022/03/01 06:00
MHDA- 2022/03/01 06:01
PMCR- 2022/02/11
CRDT- 2022/02/28 05:33
PHST- 2021/10/29 00:00 [received]
PHST- 2022/01/11 00:00 [accepted]
PHST- 2022/02/28 05:33 [entrez]
PHST- 2022/03/01 06:00 [pubmed]
PHST- 2022/03/01 06:01 [medline]
PHST- 2022/02/11 00:00 [pmc-release]
AID - 10.3389/fphys.2022.803445 [doi]
PST - epublish
SO  - Front Physiol. 2022 Feb 11;13:803445. doi: 10.3389/fphys.2022.803445. eCollection 
      2022.