线粒体动力学及线粒体自噬在感音神经性耳聋分子机制中的作用OA

Mitochondria are crucial for the body's energy metabolism.Mitochondrial dysfunction can lead to abnormal cellular energy metabolism,causing cell death or functional decline,which can then lead to fundamental pathological changes in certain diseases.Currently,the academic community generally believes that mitochondrial damage may be one of the main pathogenic mechanisms of sensorineural hearing loss(SNHL).Numerous studies have shown that mitochondrial dysfunction,such as mitochondrial dynamics disorders,autophagy impairment,or mitochondrial DNA mutations,can result in accumulation of reactive oxygen species,which,through oxidative stress,can damage cells in the auditory conduction pathway,such as auditory nerves and cochlear hair cells,ultimately progressing to SNHL.Presbycusis,the most common type of SNHL,is closely associated with functional decline of the mitochondrial quality control system,manifested as mitochondrial dynamics imbalance and reduced autophagy.This article aims to introduce and summarize the research progress on the mitochondrial quality control system in SNHL,with particular emphasis on presbycusis.