Special issue: Neuroinflammatory pathways as treatment targets in brain disorders autophagic regulation of neuroinflammation in ischemic stroke.

Abstract Despite the high lethality and increasing prevalence, effective therapy for ischemic stroke is still limited. As a crucial pathophysiological mechanism underlying ischemic injury, neuroinflammation remains a promising target for novel anti-ischemic strategies. However, the potential adverse effects limit the applications of traditional anti-inflammatory therapies. Recent explorations into the mechanisms of inflammation reveal that autophagy acts as a critical part in inflammation regulation. Autophagy refers to the hierarchically organized process resulting in the lysosomal degradation of intracellular components. Autophagic clearance of intracellular danger signals (DAMPs) suppresses the inflammation activation. Alternatively, autophagy blunts inflammation by removing either inflammasomes or the transcriptional modulators of cytokines. Interestingly, several compounds have been proved to alleviate neuroinflammatory responses and protect against ischemic injury by activating autophagy, highlighting autophagy as a promising target for the regulation of ischemia-induced neuroinflammation. Nonetheless, the molecular mechanism underlying autophagic regulation of neuroinflammation in the central nervous system is less clear and further explorations are still needed.