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生物力学因素与椎间盘退变之间的关系:综述

The relationship between biomechanical factors and intervertebral disc degeneration: a review.

作者信息

Meng Zhenyu, Tan Jinhua, Ouyang Xueqian, Yin Jian, Yan Yiguo

机构信息

Department of Spine Surgery, The First Affiliated Hospital of University of South China Hengyang 421000, Hunan, China.

Affiliated Nanhua Hospital, University of South China Hengyang 421000, Hunan, China.

出版信息

Am J Transl Res. 2025 May 15;17(5):3575-3585. doi: 10.62347/DSJK1156. eCollection 2025.

DOI:10.62347/DSJK1156
PMID:40535657
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12170379/
Abstract

The intervertebral disc is an avascular structure composed of the nucleus pulposus, annulus fibrosus, and the superior and inferior cartilage endplates. Located between adjacent vertebrae, it connects them structurally, contributing to spinal stability, load-bearing, shock absorption, and protection of the spinal cord. Intervertebral disc degeneration (IDD) results from various factors, including mechanical overload, trauma, repetitive strain, pregnancy, genetic predisposition, and developmental abnormalities. In the context of increased occupational demands and lifestyle changes, the spine is subjected to greater biomechanical stress, accelerating disc degeneration; increasing the risk of lumbar disc herniation. This review summarizes current knowledge on how biomechanical factors contribute to IDD, focusing on the involvement of mechanical stimuli in cellular and molecular pathways. It highlights both the detrimental and potentially protective effects of biomechanical forces on intervertebral discs and their resident cells. By exploring the dual roles of these forces, this review aims to inform future research directions and therapeutic strategies. Taken together, the evidence underscores a strong relationship between biomechanical loading and intervertebral disc degeneration at both the tissue and cellular levels.

摘要

椎间盘是一种无血管结构,由髓核、纤维环以及上下软骨终板组成。它位于相邻椎体之间,在结构上连接椎体,有助于脊柱稳定、承重、减震以及保护脊髓。椎间盘退变(IDD)由多种因素引起,包括机械性过载、创伤、反复劳损、妊娠、遗传易感性和发育异常。在职业需求增加和生活方式改变的背景下,脊柱承受更大的生物力学应力,加速椎间盘退变,增加腰椎间盘突出症的风险。本综述总结了关于生物力学因素如何导致IDD的现有知识,重点关注机械刺激在细胞和分子途径中的作用。它强调了生物力学力对椎间盘及其驻留细胞的有害和潜在保护作用。通过探讨这些力的双重作用,本综述旨在为未来的研究方向和治疗策略提供信息。综上所述,证据强调了生物力学负荷与椎间盘退变在组织和细胞水平上的密切关系。

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本文引用的文献

1
Activation of JNK/p38 MAPK Signaling Pathway by lncRNA DGCR5 Promotes Nucleus Pulposus Cell Degeneration and Pyroptosis in Intervertebral Disk Degeneration.lncRNA DGCR5激活JNK/p38 MAPK信号通路促进椎间盘退变中髓核细胞的退变和焦亡
Neurosurgery. 2025 Mar 25;97(3):752-761. doi: 10.1227/neu.0000000000003406.
2
Stress-Activated Protein Kinases in Intervertebral Disc Degeneration: Unraveling the Impact of JNK and p38 MAPK.椎间盘退变中的应激激活蛋白激酶:揭示JNK和p38丝裂原活化蛋白激酶的影响
Biomolecules. 2024 Mar 25;14(4):393. doi: 10.3390/biom14040393.
3
Aberrant mechanical loading induces annulus fibrosus cells apoptosis in intervertebral disc degeneration via mechanosensitive ion channel Piezo1.异常的机械负荷通过机械敏感离子通道 Piezo1 诱导椎间盘退变中的纤维环细胞凋亡。
Arthritis Res Ther. 2023 Jul 7;25(1):117. doi: 10.1186/s13075-023-03093-9.
4
Mechanical Stretch Induced Osteogenesis on Human Annulus Fibrosus Cells through Upregulation of BMP-2/6 Heterodimer and Activation of P38 and SMAD1/5/8 Signaling Pathways.机械拉伸通过上调 BMP-2/6 异二聚体和激活 P38 和 SMAD1/5/8 信号通路诱导人纤维环细胞成骨。
Cells. 2022 Aug 20;11(16):2600. doi: 10.3390/cells11162600.
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Mechanical Stretch-Induced NLRP3 Inflammasome Expression on Human Annulus Fibrosus Cells Modulated by Endoplasmic Reticulum Stress.机械拉伸诱导人纤维环细胞 NLRP3 炎性小体表达受内质网应激调控。
Int J Mol Sci. 2022 Jul 19;23(14):7951. doi: 10.3390/ijms23147951.
6
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JOR Spine. 2022 Mar 10;5(2):e1197. doi: 10.1002/jsp2.1197. eCollection 2022 Jun.
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Arthritis Res Ther. 2022 May 23;24(1):119. doi: 10.1186/s13075-022-02804-y.
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