摘要
The mammalian/mechanistic target of rapamycin(m TOR) is a serine/threonine protein kinase that integrates inputs from nutrients and growth factors to control many fundamental cellular processes through two distinct protein complexes m TORC1 and m TORC2.Recent mouse genetic studies have established that m TOR pathways play important roles in regulating multiple aspects of skeletal development and homeostasis. In addition, m TORC1 has emerged as a common effector mediating the bone anabolic effect of Igf1,Wnt and Bmp. Dysregulation of m TORC1 could contribute to various skeletal diseases including osteoarthritis and osteoporosis.Here we review the current understanding of m TOR signaling in skeletal development and bone homeostasis, as well as in the maintenance of articular cartilage. We speculate that targeting m TOR signaling may be a valuable approach for treating skeletal diseases.
The mammalian/mechanistic target of rapamycin(m TOR) is a serine/threonine protein kinase that integrates inputs from nutrients and growth factors to control many fundamental cellular processes through two distinct protein complexes m TORC1 and m TORC2.Recent mouse genetic studies have established that m TOR pathways play important roles in regulating multiple aspects of skeletal development and homeostasis. In addition, m TORC1 has emerged as a common effector mediating the bone anabolic effect of Igf1,Wnt and Bmp. Dysregulation of m TORC1 could contribute to various skeletal diseases including osteoarthritis and osteoporosis.Here we review the current understanding of m TOR signaling in skeletal development and bone homeostasis, as well as in the maintenance of articular cartilage. We speculate that targeting m TOR signaling may be a valuable approach for treating skeletal diseases.
基金
funded by the National Key R&D Program of China (2016YFC1100203) (J. C.)
the Priority Academic Program Development of Jiangsu High Education Institutions (PAPD) (J.C.)
the National Natural Science Foundation of China (81772294) (J.C.)
NIH R01 AR060456 and R01 AR055923 (F.L.)
