Crosstalk between reactive oxygen species mediated programmed cell death of nucleus pulposus cells.

It is yet unknown what causes intervertebral disc degeneration (IVDD), a chronic inflammatory systemic illness. Lower back pain may result from the disease's primary pathogenic characteristic, which is the degeneration of nucleus pulposus cells (NPCs). While IVDD can currently be improved by medications, there are still serious toxic side effects that require immediate attention. Consequently, the identification of novel therapeutic targets depends on a thorough examination of the mechanisms underlying the onset and progression of IVDD. Particularly in NPCs, annulus fibrosus, and cartilage endplate cells, where programmed cell death (PCD) dysregulation is particularly crucial. This article summarizes the various forms of PCD, including apoptosis, necroptosis, autophagy, which have been extensively studied, as well as the regulatory roles of newly discovered NETosis, pyroptosis, ferroptosis, cuproptosis, etc. in IVDD, and explores their regulatory roles in NPCs and others. These results indicate the direction for the development of novel target medications in addition to offering a crucial theoretical foundation for improving the clinical treatment strategy for IVDD.