Stroke is the leading cause of death and adult disability worldwide. Mitochondrial dysfunction has been regarded as one of the hallmarks of ischemia/reperfusion (I/R) induced neuronal death. Maintaining the function of mitochondria is crucial in promoting neuron survival and neurological improvement. In this article, we review current progress regarding the roles of mitochondria in the pathological process of cerebral I/R injury. In particular, we emphasize on the most critical mechanisms responsible for mitochondrial quality control, as well as the recent findings on mitochondrial transfer in acute stroke. We highlight the potential of mitochondria as therapeutic targets for stroke treatment and provide valuable insights for clinical strategies.

Hydroxyl radical (•OH) and singlet oxygen (1O2) were detected by electron spin resonance (ESR) spectroscopy in a direct current He/O2 (2%) non‐thermal plasma microjet‐water system. ${}^{ \bullet }{\rm O}_{{\rm 2}}^{- } $ is shown to be the precursor of •OH. The concentrations of 1O2 and •OH are evaluated to be around 6 × 10−4 and 1.2 × 10−5 M, respectively. The survival rates of S. aureus exposed to plasma for 20 s in 1 ml H2O, SOD (100 U, for scavenging ${}^{ \bullet }{\rm O}_{{\rm 2}}^{- } $), D‐Man (0.15 M, for scavenging •OH), and L‐His (0.15 M, for scavenging •OH and 1O2) solutions were 0.7, 1.6, 13.4, and 40.9%, respectively, indicating that 1O2 contributes the most to the inactivation.

Scheme 1. Hydroxylation of C sp 2ÀH bonds. BQ = benzoquinone, DG = directing group.

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