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Crosstalk between reactive oxygen species mediated programmed cell death of nucleus pulposus cells
Chaoqi Chen1, Xiaofei Wu1, Baoxin Shen1
1Department of Orthopedics, RuiKang Hospital Affiliated to Guangxi University of Chinese Medicine, Nanning, Guangxi Province, China.
Abstract:
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.
Insights
Intervertebral disc degeneration (IVDD) mechanisms remain unclear. This review explores programmed cell death (PCD) pathways in IVDD, offering insights for novel therapeutic targets and improved clinical strategies for lower back pain.
Area of Science:
- Biomedical Science
- Cell Biology
- Pathology
Background:
- Intervertebral disc degeneration (IVDD) is a chronic inflammatory condition causing lower back pain.
- The degeneration of nucleus pulposus cells (NPCs) is a key feature of IVDD.
- Current treatments for IVDD have significant toxic side effects.
Purpose of the Study:
- To investigate the mechanisms underlying the onset and progression of IVDD.
- To identify novel therapeutic targets for IVDD.
- To explore the role of programmed cell death (PCD) in IVDD.
Main Methods:
- Literature review of programmed cell death (PCD) pathways.
- Analysis of PCD's role in nucleus pulposus cells (NPCs), annulus fibrosus, and cartilage endplate cells.
- Summary of known and emerging PCD types, including apoptosis, necroptosis, autophagy, NETosis, pyroptosis, ferroptosis, and cuproptosis.
Main Results:
- Dysregulation of PCD is crucial in IVDD pathogenesis.
- Various PCD pathways, both classical and novel, are implicated in IVDD.
- Understanding these PCD mechanisms provides a foundation for developing new treatments.
Conclusions:
- Programmed cell death (PCD) dysregulation is a critical factor in intervertebral disc degeneration (IVDD).
- Emerging PCD pathways like NETosis, pyroptosis, ferroptosis, and cuproptosis warrant further investigation in IVDD.
- This research provides a theoretical basis for developing targeted therapies to improve IVDD treatment.
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