Osteoclasts control endochondral ossification via regulating acetyl-CoA availability  

作　　者：Daizhao Deng Xianming Liu Wenlan Huang Sirui Yuan Genming Liu Shanshan Ai Yijie Fu Haokun Xu Xinyi Zhang Shihai Li Song Xu Xiaochun Bai Yue Zhang 

机构地区：[1]Department of Cell Biology,School of Basic Medical Science,Southern Medical University,Guangzhou 510515 Guangdong,China [2]Department of Physiology,School of Basic Medical Science,Southern Medical University,Guangzhou 510515 Guangdong,China [3]Department of Orthopaedics,Nanfang Hospital,Southern Medical University,Guangzhou 510515 Guangdong,China

出　　处：《Bone Research》2024年第3期720-733,共14页骨研究（英文版）

基　　金：supported by Grant Nos.31872799,82070906 and 31701033 from the National Natural Science Foundation of China;Grant Nos.2020A1515011189 from Guangdong Basic and Applied Basic Research Foundation of China。

摘　　要：Osteoclast is critical in skeletal development and fracture healing,yet the impact and underlying mechanisms of their metabolic state on these processes remain unclear.Here,by using osteoclast-specific small GTPase Rheb1-knockout mice,we reveal that mitochondrial respiration,rather than glycolysis,is essential for cathepsin K(CTSK)production in osteoclasts and is regulated by Rheb1 in a mechanistic target of rapamycin complex 1(mTORC1)-independent manner.

关 键 词：HEALING SKELETAL CATHEPSIN 

分 类 号：R68[医药卫生—骨科学]