Abstract
Ischemic stroke, the second leading cause of human mortality, presents a formidable challenge to healthcare. Following ischemic insult, the brain undergoes intricate pathological transformations, prominently marked by mitochondrial damage, including swelling, fission, and mitophagy, collectively termed mitochondrial quality control disorder. Mitochondria, pivotal in energy regulation and oxidative stress modulation, play a critical role in neuronal apoptosis post-stroke. To solve the problems caused by mitochondrial quality control disorders, mitochondrial transfer has become a new therapeutic strategy for central nervous system diseases. Mitochondrial transfer refers to the process by which certain cell types export their mitochondria and pass them on to other cell types, a process also known as intercellular mitochondrial transfer. Mechanistically, mitochondrial transfer occurs via tunneling nanotubes, extracellular vesicles, and free mitochondrial transfer, exerting multifaceted effects such as anti-inflammatory, anti-lipid peroxidation, ferroptosis modulation, and enhancement of mitochondrial metabolism. This review explores the therapeutic efficacy, current obstacles, and future prospects of mitochondrial transfer in ischemic stroke, offering insights to researchers and instilling hope in patients for conquering this debilitating condition.