PI3K/AKT信号通路调控DDH脱位后软骨细胞自噬的相关研究  

Research on the Regulation of Chondrocyte Autophagy after DDH Dislocation by the PI3K/AKT Signaling Pathway

作　　者：郭宇 祁凯 陈云鹏 黄志明 王伟豪 韦宜山[1] 

机构地区：[1]内蒙古医科大学第二附属医院,内蒙古 呼和浩特

出　　处：《临床医学进展》2024年第4期2385-2389,共5页Advances in Clinical Medicine

摘　　要：发育性髋关节脱位(development dislocation of the hip, DDH),是在髋关节发育不良的基础上,伴有或不伴有股骨头脱位或半脱位于髋臼之外的下肢畸形。其病理改变不同可能会导致严重程度不一的早期骨关节炎(osteoarthritis, OA)。DDH的一个重要病理变化是关节软骨的退化及退变,但目前关于DDH软骨退变的机制尚未明确。一些研究发现软骨细胞的自噬与骨关节炎密切相关,其中PI3K/AKT信号通路可以促进软骨细胞增殖,并且抑制软骨细胞自噬。本文旨在探讨PI3K/AKT信号通路对软骨细胞自噬的调控作用,为DDH后期的诊疗提供新的思路。Developmental dislocation of the hip (DDH) is a lower limb deformity located outside the acetabulum, with or without dislocation or subluxation of the femoral head, on the basis of hip dysplasia. Different pathological changes may lead to early osteoarthritis (OA) with varying degrees of severity. One important pathological change of DDH is the degradation and degeneration of articular cartilage, but the mechanism of DDH cartilage degeneration is currently unclear. Some studies have found that autophagy of chondrocytes is closely related to osteoarthritis, among which the PI3K/AKT signaling pathway can promote chondrocyte proliferation and inhibit chondrocyte autophagy. This article aims to explore the regulatory role of the PI3K/AKT signaling pathway on chondrocyte autophagy, providing new ideas for the diagnosis and treatment of DDH in the later stage.

关 键 词：PI3K/AKT 发育性 髋关节脱位 自噬 软骨细胞 

分 类 号：R68[医药卫生—骨科学]