Wu Ruixia, Zhao Xiao Juan, Du Yaxin, Dong Yizhi, Song Xinyue, Zhu Yong
Inner Mongolia Medical University, Hohhot, China.
The Second Affiliated Hospital of Inner Mongolia Medical University, Hohhot, China.
Front Nutr. 2025 Mar 10;12:1533264. doi: 10.3389/fnut.2025.1533264. eCollection 2025.
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 disk 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. Intervertebral disks are essential for maintaining spinal alignment. Their primary functions encompass shock absorption, preservation of physiological curvature, facilitation of movement, and provision of stability. The elasticity and thickness of these disks effectively absorb daily impacts, safeguard the spine, uphold its natural curvature and flexibility, while also creating space for nerve roots to prevent compression and ensure normal transmission of nerve signals. 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 disks, NP is essential for maintaining disk 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 disks. 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.
脂质代谢涵盖生物系统内脂肪的消化、吸收、合成和降解过程，在维持正常生理功能中起着关键作用。脂质代谢紊乱以血脂水平异常和脂肪酸代谢失调为特征，已成为椎间盘退变（IDD）的重要促成因素。IDD的发病机制是多方面的，包括遗传易感性、营养和代谢因素、机械应激源、创伤和炎症反应，这些因素共同促进了IDD的进展。尽管IDD的确切机制仍未完全阐明，但脂质代谢紊乱与其发展之间的密切关联已达成广泛共识。椎间盘对于维持脊柱排列至关重要。其主要功能包括减震、保持生理曲度、促进运动以及提供稳定性。这些椎间盘的弹性和厚度可有效吸收日常冲击，保护脊柱，维持其天然曲度和灵活性，同时还为神经根创造空间以防止受压并确保神经信号的正常传递。研究表明，这种代谢紊乱可能损害软骨终板（CEP）和髓核（NP）的功能，从而促进IDD的发生和发展。CEP对于内部物质交换和减震至关重要，同时在机械负荷条件下减轻NP突出。作为椎间盘的核心组成部分，NP对于维持椎间盘高度和提供减震能力至关重要；因此，这些关键结构的损伤会加速IDD的进展。此外，脂质代谢紊乱通过多种机制导致IDD，包括激活内质网应激途径、提高氧化应激水平、诱导细胞焦亡以及抑制自噬过程，同时促进炎症诱导的纤维化和成纤维细胞增殖，导致椎间盘内钙化。本综述阐述了脂质代谢紊乱与IDD之间的复杂相互作用；预计在未来研究中加深对这种发病机制的理解将为针对IDD的更有效预防措施和治疗策略铺平道路。
