PMID- 35153669
OWN - NLM
STAT- PubMed-not-MEDLINE
LR  - 20220215
IS  - 1662-5099 (Print)
IS  - 1662-5099 (Electronic)
IS  - 1662-5099 (Linking)
VI  - 14
DP  - 2021
TI  - Mitochondrial Quality Control: A Pathophysiological Mechanism and Therapeutic 
      Target for Stroke.
PG  - 786099
LID - 10.3389/fnmol.2021.786099 [doi]
LID - 786099
AB  - Stroke is a devastating disease with high mortality and disability rates. 
      Previous research has established that mitochondria, as major regulators, are 
      both influenced by stroke, and further regulated the development of poststroke 
      injury. Mitochondria are involved in several biological processes such as energy 
      generation, calcium homeostasis, immune response, apoptosis regulation, and 
      reactive oxygen species (ROS) generation. Meanwhile, mitochondria can evolve into 
      various quality control systems, including mitochondrial dynamics (fission and 
      fusion) and mitophagy, to maintain the homeostasis of the mitochondrial network. 
      Various activities of mitochondrial fission and fusion are associated with 
      mitochondrial integrity and neurological injury after stroke. Additionally, 
      proper mitophagy seems to be neuroprotective for its effect on eliminating the 
      damaged mitochondria, while excessive mitophagy disturbs energy generation and 
      mitochondria-associated signal pathways. The balance between mitochondrial 
      dynamics and mitophagy is more crucial than the absolute level of each process. A 
      neurovascular unit (NVU) is a multidimensional system by which cells release 
      multiple mediators and regulate diverse signaling pathways across the whole 
      neurovascular network in a way with a high dynamic interaction. The turbulence of 
      mitochondrial quality control (MQC) could lead to NVU dysfunctions, including 
      neuron death, neuroglial activation, blood-brain barrier (BBB) disruption, and 
      neuroinflammation. However, the exact changes and effects of MQC on the NVU after 
      stroke have yet to be fully illustrated. In this review, we will discuss the 
      updated mechanisms of MQC and the pathophysiology of mitochondrial dynamics and 
      mitophagy after stroke. We highlight the regulation of MQC as a potential 
      therapeutic target for both ischemic and hemorrhagic stroke.
CI  - Copyright (c) 2022 Yang, He, Deng, Xiao, Tian, Xin, Lu, Zhao and Gong.
FAU - Yang, Miaoxian
AU  - Yang M
AD  - Department of Critical Care Medicine, Huashan Hospital, Fudan University, 
      Shanghai, China.
FAU - He, Yu
AU  - He Y
AD  - Department of Critical Care Medicine, Huashan Hospital, Fudan University, 
      Shanghai, China.
FAU - Deng, Shuixiang
AU  - Deng S
AD  - Department of Critical Care Medicine, Huashan Hospital, Fudan University, 
      Shanghai, China.
FAU - Xiao, Lei
AU  - Xiao L
AD  - The State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain 
      Science, The Institutes of Brain Science, Fudan University, Shanghai, China.
FAU - Tian, Mi
AU  - Tian M
AD  - Department of Critical Care Medicine, Huashan Hospital, Fudan University, 
      Shanghai, China.
FAU - Xin, Yuewen
AU  - Xin Y
AD  - Department of Critical Care Medicine, Huashan Hospital, Fudan University, 
      Shanghai, China.
FAU - Lu, Chaocheng
AU  - Lu C
AD  - Department of Critical Care Medicine, Huashan Hospital, Fudan University, 
      Shanghai, China.
FAU - Zhao, Feng
AU  - Zhao F
AD  - Department of Critical Care Medicine, Huashan Hospital, Fudan University, 
      Shanghai, China.
FAU - Gong, Ye
AU  - Gong Y
AD  - Department of Critical Care Medicine, Huashan Hospital, Fudan University, 
      Shanghai, China.
AD  - Department of Neurosurgery, Huashan Hospital, Fudan University, Shanghai, China.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20220128
PL  - Switzerland
TA  - Front Mol Neurosci
JT  - Frontiers in molecular neuroscience
JID - 101477914
PMC - PMC8832032
OTO - NOTNLM
OT  - fission
OT  - fusion
OT  - mitochondrial quality control
OT  - mitophagy
OT  - neurovascular unit
OT  - stroke
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- 2022/02/15 06:00
MHDA- 2022/02/15 06:01
PMCR- 2021/01/01
CRDT- 2022/02/14 05:29
PHST- 2021/09/29 00:00 [received]
PHST- 2021/12/21 00:00 [accepted]
PHST- 2022/02/14 05:29 [entrez]
PHST- 2022/02/15 06:00 [pubmed]
PHST- 2022/02/15 06:01 [medline]
PHST- 2021/01/01 00:00 [pmc-release]
AID - 10.3389/fnmol.2021.786099 [doi]
PST - epublish
SO  - Front Mol Neurosci. 2022 Jan 28;14:786099. doi: 10.3389/fnmol.2021.786099. 
      eCollection 2021.