Figure 4.

S-Glutathionylation and S-Nitrosylation orchestrate mitochondrial dynamics. Under acute stress, the S-glutathionylation of MFN2 and, in turn, the oligomerization of OPA1 trigger hyperfusion as an adaptive mechanism, whereas the excessive hyper-elongation of mitochondria under aberrant S-glutathionylation leads to cell senescence. The NO-mediated S-nitrosylation of DRP1 triggers its activation and phosphorylation, which in turn activates the fission machinery to eliminate damaged mitochondria. Under excessive NO production, the hyper-fragmentation of mitochondria leads to cytochrome c release and apoptosis. Created with BioRender.com.