ABSTRACT
After ischemic stroke, the key to reduce the mortality and disability rate is to restore the blood supply of brain tissue as soon as possible. However, the cerebral ischemia-reperfusion injury (CIRI) caused by blood flow restoration is also an important cause of brain tissue structural damage and dysfunction. Studies in recent years have shown that the activation of mitophagy at CIRI stage can reduce the volume of cerebral infarction and protect neurons from CIRI, while excessive or insufficient mitophagy can aggravate CIRI. This suggests that inducing moderate mitophagy may be a potential therapeutic target for neuroprotection after stroke. However, the neuroprotective mechanism of mitophagy has not yet been fully elucidated. This article reviews the neuroprotective mechanism and potential application of mitophagy in stroke, and discusses some problems of mitophagy as a therapeutic target for stroke.
ABSTRACT
Ischemic stroke is one of the main causes of disability and death. Although intravenous thrombolysis and endovascular mechanical thrombectomy can achieve cerebral vascular recanalization, most patients with ischemic stroke leave serious neurological deficits due to missed treatment window. Neural plasticity is the basis of neural function repair. Recent studies have shown that microRNAs play an indispensable role in regulating neural plasticity. This article reviews the regulatory role of microRNAs on neural plasticity in ischemic stroke, in order to provide reference for the treatment of ischemic stroke.