Interleukin-17A (IL-17A) plays an important role in the progression of ischemic stroke. IL-17A mediates the endothelial inflammatory response, promotes water and sodium retention, and changes the electrophysiological structure of the atrium, accelerating the progression of ischemic stroke risk factors such as atherosclerotic plaques, hypertension, and atrial fibrillation. In the acute phase of ischemic stroke, IL-17A mediates neuronal injury through neutrophil chemotaxis to the site of injury, the induction of neuronal apoptosis, and activation of the calpain-TRPC-6 (transient receptor potential channel-6) pathway. During ischemic stroke recovery, IL-17A, which is mainly derived from reactive astrocytes, promotes and maintains the survival of neural precursor cells (NPCs) in the subventricular zone (SVZ), neuronal differentiation, and synapse formation and participates in the repair of neurological function. Therapies targeting IL-17A-associated inflammatory signaling pathways can reduce the risk of ischemic stroke and neuronal damage and are a new therapeutic strategy for ischemic stroke and its risk factors. In this paper, we will briefly discuss the pathophysiological role of IL-17A in ischemic stroke risk factors, acute and chronic inflammatory responses, and the potential therapeutic value of targeting IL-17A.
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