DNA甲基化在椎间盘退变中对免疫微环境的作用与机制的研究进展
Research Advances on the Role and Mechanisms of DNA Methylation in the Immune Microenvironment during Intervertebral Disc Degeneration
摘要: 椎间盘退变(IDD)作为慢性下腰痛的重要成因,其机制错综复杂,缺乏根源性的解决方案。近年来研究发现,表观遗传学修饰之DNA甲基化同IDD的进展有着极为紧密的联系。DNA甲基化不仅通过基因表达来实现对免疫微环境的精细调控,还影响着免疫细胞的极化状态及其功能表现。本文主要探讨DNA甲基化如何在IDD中影响免疫细胞(如巨噬细胞、T细胞等)的行为模式及相关免疫反应,并通过全基因组甲基化检测技术筛选出具有潜力的DNA甲基化标识物,通过结合免疫细胞浸润水平,进一步阐明DNA甲基化对椎间盘免疫微环境的调控作用机理,旨在为IDD的早期筛查诊断及靶向治疗打开全新的视野并提出可行路径。
Abstract: Intervertebral disc degeneration (IDD), a predominant cause of chronic low back pain which lacks effective therapies due to its complex pathogenesis. Growing evidence positions DNA methylation as a central epigenetic regulator in IDD, governing both immune gene networks and cellular functionality. This study elucidates how methylation remodels immune responses by controlling macrophage polarization and T-cell differentiation within degenerative discs. This study investigates how DNA methylation modulates the functional dynamics and immune activation profiles of key immune cells (including macrophages and T lymphocytes) in inter-vertebral disc degeneration (IDD). Employing genome-wide methylation profiling, we systematically identify disease-associated DNA methylation biomarkers while elucidating their regulatory impact on immune microenvironment remodeling. Through integration of quantitative immune infiltration mapping, we systematically decipher the epigenetic regulatory networks through which DNA methylation orchestrates intervertebral disc immune microenvironments. This mechanistic exploration establishes a novel diagnostic-therapeutic framework that enables precision strategies for early detection, molecular subtyping, and pathway-specific interventions in IDD management.
文章引用:伟乐斯, 包志斌, 高岗, 杨物鹏. DNA甲基化在椎间盘退变中对免疫微环境的作用与机制的研究进展[J]. 临床医学进展, 2025, 15(4): 1754-1761. https://doi.org/10.12677/acm.2025.1541118

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