Abstract：
:Recovered blood supply after cerebral ischemia for a certain period of time fails to restore brain function, with more severe dysfunctional problems developing, called cerebral ischemia-reperfusion injury (CIR). CIR involves several extremely complex pathophysiological processes in which the interactions between key factors at various stages have not been fully elucidated. Mitochondrial dysfunction is one of the most important mechanisms of CIR. The mitochondrial deacetylase, sirtuin 3 (SIRT3), can inhibit mitochondrial oxidative stress by deacetylation, to maintain mitochondrial stability. Uncoupling protein 2 (UCP2) regulates ATP (Adenosine triphosphate) and reactive oxygen species production by affecting the mitochondrial respiratory chain, which may play a protective role in CIR. Finally, we propose that UCP2 regulates the activity of SIRT3 through sensing the energy level and, in turn, maintaining the mitochondrial steady state, which demonstrates a cytoprotective effect on CIR.
journal_name
Int J Mol Scijournal_title
International journal of molecular sciencesauthors
Su J,Liu J,Yan XY,Zhang Y,Zhang JJ,Zhang LC,Sun LKdoi
10.3390/ijms18071599subject
Has Abstractpub_date
2017-07-24 00:00:00issue
7issn
1422-0067pii
ijms18071599journal_volume
18pub_type
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