股骨头坏死信号通路研究概述

Summary of the signaling pathway of osteonecrosis of femoral head

股骨头坏死是一个病理演变过程,初始发生在股骨头的负重区,在应力作用下骨小梁结构发生损伤,随后针对损伤骨组织进行修复,造成骨坏死的外因不消除,修复不完善,损伤-修复的过程继续发展将导致股骨头结构改变,出现塌陷、变形,导致关节炎症、功能障碍等结果。该病的发病与头部的缺血和细胞的凋亡有关。大量研究发现该病的发生发展机制是一个复杂的作用网络,与多条信号通路相关,各类信号通路可以通过调控成骨细胞、破骨细胞或者血管生成素等靶点影响股骨头坏死进程。本文通过梳理大量基础研究,总结了TGF-β/BMP/Smad、AMPK、Wnt/β-catenin、OPG/RANKL/RANK、PI3K/Akt/mTOR和TLR4/NF-κB六条与股骨头坏死密切相关的细胞信号通路,以期为临床股骨头坏死的治疗和研究提供参考。

Necrosis of femoral head is a pathological process,the initial occurred in the weight-bearing area of the femoral head,the pressure under the action of damage in the trabecular bone structure of femoral head,then in view of the bone tissue repair damage,cause osteonecrosis of the external cause is not eliminated,repair is not perfect,damage repair process to continue to develop will trigger a femoral head structure change,subsidence and deformation,lead to joint inflammation,dysfunction and other results.The pathogenesis of this disease is related to ischemia of the head and apoptosis of cells.A large number of studies have found that the pathogenesis of the disease is a complex network of action,which is related to multiple signaling pathways,and various signaling pathways can affect the process of the disease by regulating osteoblasts,osteoclasts,angiopoietin and other targets.In this paper,six signaling pathways,including TGF-β/BMP/Smad,AMPK,Wnt/β-catenin,OPG/RANKL/RANK,PI3K/Akt/mTOR and TLR4/NF-κB,which are closely related to femoral head necrosis,were summarized by reviewing some basic studies.In order to provide reference for clinical treatment and research of femoral head necrosis.