基于V-ATPase a3转运蛋白探讨骨质疏松症的分子机制  

Exploration of the molecular mechanism of osteoporosis based on the V-ATPase a3 transporter

作　　者：宋敏[1] 陈秉雄 陈秉虎 柴居堂 董万涛[3] 蒋宜伟[3] 

机构地区：[1]甘肃中医学院,兰州730000 [2]临洮县人民医院,甘肃定西730500 [3]甘肃中医学院附属医院,兰州730020

出　　处：《中国骨质疏松杂志》2014年第6期706-710,共5页Chinese Journal of Osteoporosis

基　　金：甘肃省财政厅基本科研项目(BH2010-028);甘肃省自然科学基金项目(1010RJZA160)

摘　　要：目的存在于破骨细胞的皱褶缘上的V-ATPase a3转运蛋白在骨质疏松症的骨吸收中发挥着重要作用。V-ATPase a3转运蛋白将H+逆浓度梯度转运到密闭区,溶解无机矿物质,为水解酶如CAⅡ、CATK、MMPs等提供酸性环境,抑制V-ATPase a3转运蛋白已成为治疗骨质疏松症的新靶标;并深化对CAⅡ、CATK、MMPs等水解酶阻滞剂的认识,从而多渠道、多方位、多靶点地拓展骨质疏松症的治疗。V-ATPase a3 transporter, which exists in the ruffled border of osteoclasts, plays an important role in bone resorption in osteoporosis.It can transport H＋to the closed area to form a high H＋concentration zone, thus dissolving inorganic minerals and providing an acidic environment for hydrolytic enzymes including CA II, CATK, and MMPs.The inhibitor of the V-ATPase a3 transporter has become the new target for the treatment of osteoporosis.Deep understanding of the hydrolytic enzymes including CA II, CATK, and MMPs can provide new ideas concerning the multi-channel, multi-dimension, and multi-target treatment of the osteoporosis.

关 键 词：V-ATPASE A3 破骨细胞 骨质疏松症 V-ATPASE A3 

分 类 号：R31[医药卫生—基础医学]