| 唐茂林.细胞衰老、Notch信号通路与椎间盘退变的相关研究[J].安徽医药,待发表. |
| 细胞衰老、Notch信号通路与椎间盘退变的相关研究 |
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| 投稿时间：2025-03-22 录用日期：2025-04-27 |
| DOI： |
| 中文关键词: 髓核细胞、细胞衰老、Notch信号通路、椎间盘退变 |
| 英文关键词: |
| 基金项目:国家自然科学基金(82360420)；贵州医科大学附属医院博士科研启动基金(gyfybskj-2023-07)；贵州省科技计划项目(黔科合基础-ZK[2023]一般387)；贵州省科技计划项目(黔科合基础-ZK[2024]一般222)； |
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| 摘要点击次数: 36 |
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| 中文摘要: |
| 椎间盘退变(IVDD)作为一类常见的随年龄增长而出现的退行性疾病,主要累及髓核、纤维环以及软骨终板等椎间盘重要结构,是引发慢性腰痛的核心病因。髓核(NP)细胞的变性进程受氧化应激、炎症反应、细胞凋亡、异常增殖以及自噬等一系列复杂且相互关联的病理过程驱动,其中 NP 细胞的衰老与 NP 变性的发展密切相关,端粒缩短、DNA 损伤反应、表观遗传改变等经典衰老途径也在 IVDD 的病理进程中得以验证。Notch 信号通路在几乎所有器官系统中均有表达,对细胞增殖、分化以及细胞命运的调控发挥着广泛作用。在IVDD中,Notch 信号通路活性呈现上升趋势,且在一定程度上能够延缓IVDD进展。本文系统梳理细胞衰老、Notch 信号通路以及 IVDD 发病机制等方面的研究成果,旨在为后续 IVDD 的临床治疗开拓新的思路,提供坚实的理论基础。 |
| 英文摘要: |
| Intervertebral disc degeneration (IVDD), as a common type of degenerative disease that occurs with aging, mainly affects important structures of the intervertebral disc such as the nucleus pulposus, annulus fibrosus, and cartilaginous endplate, and is the core cause of chronic low back pain. The degenerative process of nucleus pulposus (NP) cells is driven by a series of complex and interrelated pathological processes, including oxidative stress, inflammatory response, apoptosis, abnormal proliferation, and autophagy. Among them, the senescence of NP cells is closely related to the development of NP degeneration. Classic aging pathways such as telomere shortening, DNA damage response, and epigenetic changes have also been verified in the pathological process of IVDD. The Notch signaling pathway is expressed in almost all organ systems and plays a wide role in regulating cell proliferation, differentiation, and cell fate. In IVDD, the activity of the Notch signaling pathway shows an upward trend and can, to a certain extent, delay the progression of IVDD. This article systematically reviews the research achievements in the fields of cellular senescence, the Notch signaling pathway, and the pathogenesis of IVDD, aiming to open up new ideas for the subsequent clinical treatment of IVDD and provide a solid theoretical basis. |
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