The Roles of Autophagy and Inflammatory Responses in Acute Ischemic Stroke

Autophagy and inflammation play a key role in the pathogenesis of ischemic stroke; the latest research shows that autophagy and inflammation are seen as a doubleedged sword. Insufficient or excessive autophagy will cause nerve damage, promote cell death, while the moderately autophagy has a neuroprotective effect. After the occurrence of ischemic stroke, the inflammatory response activates anti-inflammatory mediators and proinflammatory mediators, breaking the dynamic balance between proinflammatory response and anti-inflammatory response, causing detriment to the brain, affecting brain function recovery. The main purpose of this article is to systematically summarize the recent studies on autophagy and inflammatory responses in acute ischemic stroke, a brief analysis the roles of autophagy and inflammatory responses in the pathophysiology of ischemic stroke, investigate the correlation between both. To build a foundation for research on how to make autophagy and proinflammatory and anti-inflammatory responses achieve the desired balance at different stages of the stroke, in order to provide research directions for acute ischemic stroke and to form new and effective therapeutic strategies.