Qiang Wang

TL;DR: It was hypothesized that the augmentation of mitochondrial damage after cerebral ischemia could be resolved by timely replenishment of exogenous mitochondria, and the number of extracellular mitochondria increased in rat cerebrospinal fluid and a higher proportion of mitochondria were associated with good neurological outcomes.

TL;DR: EA pretreatment enhances STAT3 activation via CB1R to protect against cerebral ischemia, suggesting thatSTAT3 activation may be a novel target for stroke intervention.

TL;DR: Sevoflurane preconditioning-induced protective effects against transient cerebral ischemic injuries are mediated by the activation of canonical Notch signaling pathway in mice.

TL;DR: It is suggested that α7nAChR-dependent cholinergic anti-inflammatory system and NLRP3 inflammasome in neurons might act as potential therapeutic targets in EA induced neuroprotection against cerebral ischemic injury.

TL;DR: Findings indicate that EDA protects against kidney damage caused by ischemia–reperfusion through JAK/STAT signaling, inhibiting apoptosis and improving mitochondrial injury.