高糖调控MAPK信号通路在椎间盘退变中的研究进展

椎间盘退变(intervertebral disc degeneration，IVDD)是诱发多种脊柱疾患的病理基础，亦是腰痛发生的主要因素，严重影响患者的生活质量，给患者家庭及社会带来沉重的经济负担。糖尿病是诱发IVDD主要疾病之一。高糖生态位介导的椎间盘（IVD）细胞凋亡是糖尿病相关脊柱退行性疾病的潜在致病因素。高糖通过激活丝裂原活化蛋白激酶(MAPK)信号通路促进IVDD细胞外基质（ECM）的降解、衰老、凋亡和炎症反应，亦通过诱导自噬和氧化应激，加速IVDD的病理进程。笔者通过查阅国内外相关文献，通过综述高糖调控MAPK信号通路在IVDD中的研究进展，旨在为今后深入研究该信号通路的作用机制及阐明高糖通过调控MAPK信号通路在IVDD中的作用提供参考。

Research progress of MAPK signaling pathway regulated by high glucose in intervertebral disc degeneration

The intervertebral disc degeneration (IVDD) is induced by a variety of disorders of the spine pathological basis. It is also the main factor of the occurrence of back pain occurs. It serious influences the patient''s quality of life, leading to heavy economic burden for patient''s family and the society. Diabetes mellitus (DM) is one of the major diseases that induce IVDD. Intervertebral disc (IVD) cell apoptosis mediated by high glucose niche is a potential causative factor in diabetes-related spinal degenerative diseases. High glucose promotes the degradation, senescence, apoptosis, and inflammation of IVDD extracellular matrix (ECM) by activating mitogen activated protein kinase (MAPK) signaling pathway, and accelerates the pathological process of IVDD by inducing autophagy and oxidative stress. By referring to relevant literature at home and abroad, the authors review the research progress of MAPK signaling pathway regulated by high glucose in IVDD, aiming to provide reference for further study of the mechanism of action of this signaling pathway and to elucidate the role of high glucose regulating MAPK signaling pathway in IVDD.