[Progress on mechanism of mitochondrial autophagy in pathogenesis of intervertebral disc degeneration based on PINK1/Parkin signaling pathway].

Abstract

Intervertebral disc degeneration (IVDD) is one of the main causes of lower back pain. The chronic accumulation of aging and apoptosis of nucleus pulposus cells (NPCs) is believed to be related to IVDD. In recent years, mitochondrial autophagy which as an important clearance mechanism within cells, has gradually attracted attention. The PINK1/Parkin signaling pathway is regarded as the key pathway regulating mitochondrial autophagy, and it plays a significant role in physiological and pathological processes of NPCs. The mechanism by which PINK1/Parkin signaling pathway mediates mitochondrial autophagy could be understood as follows, PINK1, as the sensor for mitochondrial quality regulation, is activated. It recruits and activates Parkin to the mitochondrial membrane through phosphorylation of ubiquitin, and then undergoes Parkin-dependent substrate ubiquitination, recruitment of autophagy receptors, formation of autophagosomes, and fusion with lysosomes, ultimately completing the extremely important autophagy process. Current research indicates that abnormality of PINK1/Parkin signaling pathway may be closely related to IVDD, but the specific mechanism still requires further exploration. The paper explores research progress of mechanism by which mitochondrial autophagy affects IVDD based on PINK1/Parkin signaling pathway, with the aim of providing new strategies and targets for the treatment of IVDD.