PDF(Pubmed)
Abstract：
Intervertebral disc degeneration (IDD) is a major cause of lower back pain. The pathophysiological development of IDD is closely related to the stimulation of various stressors, including proinflammatory cytokines, abnormal mechanical stress, oxidative stress, metabolic abnormalities, and DNA damage, among others. These factors prevent normal intervertebral disc (IVD) development, reduce the number of IVD cells, and induce senescence and apoptosis. Stress-activated protein kinases (SAPKs), particularly, c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (p38 MAPK), control cell signaling in response to cellular stress. Previous studies have shown that these proteins are highly expressed in degenerated IVD tissues and are involved in complex biological signal-regulated processes. Therefore, we summarize the research reports on IDD related to JNK and p38 MAPK. Their structure, function, and signal regulation mechanisms are comprehensively and systematically described and potential therapeutic targets are proposed. This work could provide a reference for future research and help improve molecular therapeutic strategies for IDD.
摘要：
椎间盘退变(IDD)是下背痛的主要原因。IDD的病理生理发展与各种应激源的刺激密切相关。包括促炎细胞因子,异常机械应力，氧化应激，代谢异常，和DNA损伤,在其他人中。这些因素阻碍了正常的椎间盘（IVD）的发展，减少IVD细胞的数量，并诱导衰老和凋亡。应激激活蛋白激酶（SAPKs），特别是,c-Jun氨基末端激酶(JNK)和p38丝裂原活化蛋白激酶(p38MAPK),控制细胞信号传导以响应细胞应激。先前的研究表明，这些蛋白质在变性的IVD组织中高度表达，并参与复杂的生物信号调节过程。因此,我们总结了与JNK和p38MAPK相关的IDD的研究报告。他们的结构，函数,和信号调节机制进行了全面和系统的描述，并提出了潜在的治疗靶点。本工作可为今后的研究提供参考,有助于完善碘缺乏病的分子治疗策略。
