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细胞衰老——从免疫角度看椎间盘退变的分子机制。

Cellular senescence - Molecular mechanisms of intervertebral disc degeneration from an immune perspective.

机构信息

Department of Orthopedics and Traumatology (Trauma and Bonesetting), The Affiliated Hospital of Traditional Chinese Medicine of Southwest Medical University, Luzhou, Sichuan, China.

Luzhou Longmatan District People's Hospital, Luzhou 646000, Sichuan Province, China.

出版信息

Biomed Pharmacother. 2023 Jun;162:114711. doi: 10.1016/j.biopha.2023.114711. Epub 2023 Apr 20.


DOI:10.1016/j.biopha.2023.114711
PMID:37084562
Abstract

Intervertebral disc degeneration (IVDD) is a frequent and intractable chronic condition in orthopedics that causes enormous discomfort in patients' lives and thoughts, as well as a significant economic burden on society and the nation. As a result, understanding the pathophysiology of IVDD is critical. The pathophysiology of IVDD has been linked to numerous variables, including oxidative stress, apoptosis, matrix metalloproteinases, and inflammatory factors. Cellular senescence has recently attracted a lot of attention in the study of age-related diseases. It has been discovered that IVDD is intimately linked to human senescence, in which nucleus pulposus cell senescence may play a significant role. Previously, our group did a comprehensive and systematic clarification of the pathogenesis of IVDD from an immune perspective and discovered that the fundamental pathogenesis of IVDD is inflammatory upregulation and nucleus pulposus cell death caused by an imbalance in the immune microenvironment. In this review, we will treat nucleus pulposus cell senescence as a novelty point to clarify the pathophysiology of IVDD and further explore the probable relationship between senescence and immunity along with the dysregulation of the immunological microenvironment to propose new therapeutic approaches for IVDD.

摘要

椎间盘退行性病变(IVDD)是骨科中一种常见且棘手的慢性疾病,给患者的生活和思想带来极大的不适,并给社会和国家带来巨大的经济负担。因此,了解 IVDD 的病理生理学至关重要。IVDD 的病理生理学与许多变量有关,包括氧化应激、细胞凋亡、基质金属蛋白酶和炎症因子。细胞衰老最近在与年龄相关疾病的研究中引起了广泛关注。已经发现,IVDD 与人类衰老密切相关,其中髓核细胞衰老可能起着重要作用。此前,我们小组从免疫角度全面系统地阐明了 IVDD 的发病机制,发现 IVDD 的根本发病机制是免疫微环境失衡导致的炎症上调和髓核细胞死亡。在这篇综述中,我们将把髓核细胞衰老作为一个新的切入点来阐明 IVDD 的病理生理学,并进一步探讨衰老与免疫之间以及免疫微环境失调的可能关系,为 IVDD 提出新的治疗方法。

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引用本文的文献

[1]
CeO Nanoparticles Reduce Oxidative Stress and Delay the Degeneration of Intervertebral Disc.

Bioinorg Chem Appl. 2025-7-13

[2]
Immune microenvironment in intervertebral disc degeneration: pathophysiology and therapeutic potential.

Front Immunol. 2025-7-4

[3]
Co-morbid mechanisms of intervertebral disc degeneration and osteoporosis: biomechanical coupling and molecular pathways synergistically driving degenerative lesions.

J Orthop Surg Res. 2025-7-14

[4]
Mechanistic Interactions Driving Nucleus Pulposus Cell Senescence in Intervertebral Disc Degeneration: A Multi-Axial Perspective of Mechanical, Immune, and Metabolic Pathways.

JOR Spine. 2025-7-2

[5]
Therapeutic mechanisms of icariin in intervertebral disc degeneration: A critical narrative review.

Biochem Biophys Rep. 2025-5-15

[6]
ELF1-mediated transactivation of METTL3/YTHDF2 promotes nucleus pulposus cell senescence via m6A-dependent destabilization of E2F3 mRNA in intervertebral disc degeneration.

Cell Death Discov. 2025-6-4

[7]
Harnessing CRISPR potential for intervertebral disc regeneration strategies.

Front Bioeng Biotechnol. 2025-5-8

[8]
Molecular Subtypes and Immune Microenvironment Characterization of the Annulus Fibrosus in Intervertebral Disc Degeneration: Insights From Translation Factor-Related Gene Analysis.

JOR Spine. 2025-4-7

[9]
Analysis of Nicotine Toxicity and Mechanisms of Senescence in Nucleus Pulposus Cells Using Network Toxicology and Molecular Docking Technique.

JOR Spine. 2025-3-31

[10]
Mitochondrial DNA variation and intervertebral disc degeneration: a genotypic analysis in a South African cohort.

Mol Biol Rep. 2025-3-7

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