PMID- 36177938
OWN - NLM
STAT- MEDLINE
DCOM- 20221003
LR  - 20221003
IS  - 2095-4352 (Print)
VI  - 34
IP  - 8
DP  - 2022 Aug
TI  - [Research progress of phosphoglycerate mutase 5-mediated mitophagy and 
      necroptosis].
PG  - 890-896
LID - 10.3760/cma.j.cn121430-20220428-00431 [doi]
AB  - Mitophagy is the selective degradation of damaged mitochondria, and it is of 
      great significance to maintain the normal quantity and quality of mitochondria to 
      ensure cell homeostasis and survival. Necroptosis is a type of programmed cell 
      necrosis that can be induced by excessive mitophagy. Reactive oxygen species 
      (ROS) are produced mainly by mitochondria and can damage mitochondria. Hyperoxic 
      acute lung injury (HALI) is a serious complication of clinical oxygen therapy, 
      and its pathogenesis is not clear. Existing studies have shown that mitophagy and 
      necroptosis are involved in the occurrence of HALI. There are many mechanisms 
      regulating mitophagy and necroptosis, including tumor necrosis factor-alpha (TNF-alpha), 
      E3 ubiquitin protein ligase (PINK1/Parkin) protein pathway encoded by 
      PTEN-induced kinase 1/PARK2 gene, phosphoglycerate mutase 5 (PGAM5), etc. PGAM5 
      has been proved to be a key factor linking mitophagy and necroptosis. Previous 
      studies of our team found that the mechanism of microRNA-21-5p (miR-21-5p) 
      alleviating HALI was related to its pGAM5-mediated inhibition of mitophagy, but 
      the mechanism of PGAM5-mediated mitophagy and necroptosis remains unclear. 
      Therefore, this paper reviews the targets of PGAM5-mediated mitophagy and 
      necroptosis, in order to find clues of lung protection of pGAM5-mediated 
      mitophagy and necroptosis in HALI, and provide theoretical basis for subsequent 
      basic research.
FAU - Zhang, Jing
AU  - Zhang J
AD  - Department of Critical Care Medicine, Affiliated Hospital of Zunyi Medical 
      University, Zunyi 563000, Guizhou, China. Corresponding author: Chen Miao, Email: 
      chenmiao64@163.com.
FAU - Chen, Miao
AU  - Chen M
FAU - Liu, Xinxin
AU  - Liu X
FAU - Ren, Yingcong
AU  - Ren Y
FAU - Liu, Guoyue
AU  - Liu G
FAU - Qin, Song
AU  - Qin S
LA  - chi
PT  - Journal Article
PT  - Review
PL  - China
TA  - Zhonghua Wei Zhong Bing Ji Jiu Yi Xue
JT  - Zhonghua wei zhong bing ji jiu yi xue
JID - 101604552
RN  - 0 (MicroRNAs)
RN  - 0 (Reactive Oxygen Species)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - EC 2.3.2.27 (Ubiquitin-Protein Ligases)
RN  - EC 2.7.- (Protein Kinases)
RN  - EC 3.1.3.16 (Phosphoprotein Phosphatases)
RN  - EC 5.4.2.11 (Phosphoglycerate Mutase)
RN  - S88TT14065 (Oxygen)
SB  - IM
MH  - Humans
MH  - *MicroRNAs
MH  - *Mitophagy/genetics
MH  - Necroptosis
MH  - Necrosis
MH  - Oxygen
MH  - Phosphoglycerate Mutase
MH  - Phosphoprotein Phosphatases/genetics/metabolism
MH  - Protein Kinases/genetics/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Tumor Necrosis Factor-alpha
MH  - Ubiquitin-Protein Ligases/genetics/metabolism
EDAT- 2022/10/01 06:00
MHDA- 2022/10/04 06:00
CRDT- 2022/09/30 05:42
PHST- 2022/09/30 05:42 [entrez]
PHST- 2022/10/01 06:00 [pubmed]
PHST- 2022/10/04 06:00 [medline]
AID - 10.3760/cma.j.cn121430-20220428-00431 [doi]
PST - ppublish
SO  - Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2022 Aug;34(8):890-896. doi: 
      10.3760/cma.j.cn121430-20220428-00431.