The bidirectional role of the JAK2/STAT3 signaling pathway and related mechanisms in cerebral ischemia-reperfusion injury.

The Janus kinase 2/signal transducer and activator of transcription 3 (JAK2/STAT3) signaling pathway, a well-conserved and basic intracellular signaling cascade, is mostly inactivated under basal conditions, although it can be phosphorylated under extracellular stimulation; in addition, it can influence the transcription and expression of multiple genes involved in biological processes such as cellular growth, metabolism, differentiation, degradation and angiogenesis. The inflammatory response, apoptosis, oxidative stress and angiogenesis are the main factors involved in the pathogenesis of ischemic stroke. Numerous studies have confirmed that the JAK2/STAT3 axis can be activated rapidly by ischemic stress, which is closely related to the regulation of these important pathological processes. However, different opinions on the specific role of this signaling pathway remain. In this paper, we review and summarize previous studies on the JAK2/STAT3 pathway in ischemic stroke.