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Ischemic stroke (IS) is the most common type of stroke, accounting for approximately 60–80% of all cases. It is mainly caused by vascular occlusion, leading to ischemic necrosis of brain tissue in the affected region and resulting in neurological dysfunction in the corresponding areas. Around 75% of patients are left with varying degrees of disability after a stroke, posing a significant burden on patients, their families, and society. Additionally, the high recurrence rate of stroke presents a major challenge to patients' health.

Currently, treatment during the recovery phase of stroke primarily involves rehabilitation training and lifestyle interventions. Pharmacological treatment focuses on controlling risk factors (such as hypertension, hypercholesterolemia, and diabetes) and secondary prevention (such as antiplatelet therapy and surgical interventions). However, for patients who continue to experience neurological deficits more than six months after a stroke, there is still no universally recognized effective treatment approach.

Following cerebral ischemia, a series of complex cascade reactions occur. When blood flow is restored to the ischemic tissue, excessive free radicals can attack cells in the reperfused area, exacerbating tissue damage. This involves multiple mechanisms, including mitochondrial dysfunction, excitotoxic neurotransmitter release, blood-brain barrier disruption, oxidative stress injury, and neuroinflammatory responses. Targeted regulation of the various signaling pathways involved in this complex pathophysiological process represents a potential therapeutic strategy for improving the prognosis of ischemic stroke.

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