Regulatory mechanisms of post-translational modifications on autophagic flux in neurons following ischemic stroke.

Ischemic stroke, a serious disease that threatens to human health, is caused by insufficient blood supply due to cerebrovascular occlusion, leading to severe brain damage and neurological deficits. Numerous investigations have revealed that autophagy is extensively involved in the pathophysiological processes of ischemic stroke. Autophagy is a vital mechanism to maintain neuronal homeostasis by degradation and recycling of cytoplasmic components. It comprises a series of consecutive processes, including autophagy initiation, autophagosome formation, fusion of autophagosomes with lysosomes, and degradation of autophagic substrates within autolysosomes. Thus, autophagy is termed as autophagic flux, as well as autophagic/lysosomal signaling pathway. Several key steps in autophagic signaling pathway are prominently regulated by post-translational modifications, thereby significantly affecting neurological outcomes after ischemic stroke. However, how the post-translational modifications regulate autophagic flux to mitigate ischemic neuronal injury remains to be systematically expounded. To provide insights into the researches on the pathogenesis and neuroprotection of ischemic stroke, this article is to summarize the post-translational modifications involved in autophagic/lysosomal signaling pathway in neurons after ischemic stroke, especially highlighting the effects of acetylation and phosphorylation on post-stroke pathophysiological processes.