Unveiling the neuroprotective power: the role of autophagy in remote ischemic conditioning

A stroke is a sudden neurological impairment caused by damage to the vascular system of the central nervous system. Remote ischemic conditioning (RIC) has emerged as a promising therapeutic strategy, gaining attention for its potential to provide neuroprotection against cerebral strokes in both clinical and preclinical settings. Recent research highlights autophagy as a key element of RIC-induced neuroprotection during cerebral ischemia. Preclinical studies suggest that RIC effectively modulates key signalling pathways, including AKT/GSK-3β, AKT-Bcl-2, Transcription Factor EB (TFEB), PINK1/Parkin, and AMPK. This modulation promotes autophagy and enhances the neuroprotective effects of RIC. Furthermore, evidence from preclinical studies indicates that RIC significantly reduces inflammation, oxidative stress, and infarct size while modulating apoptotic signalling through the activation of autophagy. This article highlights recent research that illustrates the complex interplay between RIC-induced autophagy and neuroprotection, indicating that targeting these pathways may offer innovative therapeutic approaches for treating ischemic stroke.