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REVIEW article

Front. Nutr.
Sec. Nutrition and Metabolism
Volume 12 - 2025 | doi: 10.3389/fnut.2025.1533264
This article is part of the Research Topic Diet, Trace Elements, and Gut Microbiota in Bone and Cartilage Diseases View all 6 articles

Lipid Metabolic Disorders and Their Impact on Cartilage Endplate and Nucleus Pulposus Function in Intervertebral Disc Degeneration

Provisionally accepted
Ruixia Wu Ruixia Wu 1Yaxin Du Yaxin Du 1*Yizhi Dong Yizhi Dong 1*Xinyue Song Xinyue Song 1*Yong Zhu Yong Zhu 2*
  • 1 Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China
  • 2 Peking University cancer Hospital Inner Mongolia Hospital, Hohhot, China

The final, formatted version of the article will be published soon.

    Lipid metabolism encompasses the processes of digestion, absorption, synthesis, and degradation of fats within biological systems, playing a crucial role in sustaining normal physiological functions.Disorders of lipid metabolism, characterized by abnormal blood lipid levels and dysregulated fatty acid metabolism, have emerged as significant contributors to intervertebral disc degeneration (IDD). The pathogenesis of IDD is multifaceted, encompassing genetic predispositions, nutritional and metabolic factors, mechanical stressors, trauma, and inflammatory responses, which collectively facilitate the progression of IDD. Although the precise mechanisms underlying IDD remain incompletely elucidated, there is substantial consensus regarding the close association between lipid metabolism disorders and its development. Research indicates that such metabolic disturbances may compromise the functionality of cartilaginous endplates (CEP) and nucleus pulposus (NP), thereby facilitating IDD's onset and progression. The CEP is integral to internal material exchange and shock absorption while mitigating NP herniation under mechanical load conditions. As the central component of intervertebral discs, NP is essential for maintaining disc height and providing shock-absorbing capabilities; thus, damage to these critical structures accelerates IDD progression. Furthermore, lipid metabolism disorders contribute to IDD through mechanisms including activation of endoplasmic reticulum stress pathways, enhancement of oxidative stress levels, induction of cellular pyroptosis alongside inhibition of autophagy processes-coupled with the promotion of inflammation-induced fibrosis and fibroblast proliferation leading to calcification within intervertebral discs. This review delineates the intricate interplay between lipid metabolism disorders and IDD; it is anticipated that advancing our understanding of this pathogenesis will pave the way for more effective preventive measures and therapeutic strategies against IDD in future research.

    Keywords: Lipid Metabolism, Lipid metabolic disorders, Intervertebral Disc Degeneration, Cartilage endplate, Nucleus pulposus, Oxidative Stress

    Received: 23 Nov 2024; Accepted: 06 Feb 2025.

    Copyright: © 2025 Wu, Du, Dong, Song and Zhu. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

    * Correspondence:
    Yaxin Du, Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China
    Yizhi Dong, Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China
    Xinyue Song, Inner Mongolia Medical University, Hohhot, Inner Mongolia Autonomous Region, China
    Yong Zhu, Peking University cancer Hospital Inner Mongolia Hospital, Hohhot, China

    Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.