Ouyang Zhi-Hua, Wang Wen-Jun, Yan Yi-Guo, Wang Bing, Lv Guo-Hua
Department of Spine Surgery, The 2nd Xiangya Hospital of Central South University, Changsha, China.
Department of Spine Surgery, The First Affiliated Hospital, University of South China, Hengyang, China.
Oncotarget. 2017 Jun 27;8(34):57870-57881. doi: 10.18632/oncotarget.18628. eCollection 2017 Aug 22.
Intervertebral disc degeneration (IDD) is thought to be the primary cause of low back pain, a severe public health problem worldwide. Current therapy for IDD aims to alleviate the symptoms and does not target the underlying pathological alternations within the disc. Activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway protects against IDD, which is attributed to increase of ECM content, prevention of cell apoptosis, facilitation of cell proliferation, induction or prevention of cell autophagy, alleviation of oxidative damage, and adaptation of hypoxic microenvironment. In the current review, we summarize recent progression on activation and negative regulation of the PI3K/Akt signaling pathway, and highlight its impact on IDD. Targeting this pathway could become an attractive therapeutic strategy for IDD in the near future.
椎间盘退变(IDD)被认为是导致腰痛的主要原因,而腰痛是全球范围内严重的公共卫生问题。目前针对IDD的治疗旨在缓解症状,并未针对椎间盘内潜在的病理改变。磷脂酰肌醇3-激酶(PI3K)/Akt信号通路的激活可预防IDD,这归因于细胞外基质(ECM)含量增加、细胞凋亡的预防、细胞增殖的促进、细胞自噬的诱导或预防、氧化损伤的减轻以及缺氧微环境的适应。在本综述中,我们总结了PI3K/Akt信号通路激活和负调控的最新进展,并强调了其对IDD的影响。在不久的将来,靶向该信号通路可能成为一种有吸引力的IDD治疗策略。