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.
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。
