| Chemerin is a secreted adipokine plays multiple physiological or pathological functions through binding three of its cognitive receptors：CMKLR1, GPR1 or CCRL2, so that to stimulate downstream molecular events or silence chemerin signaling. Chemerin/CMKLR1 signaling was involved in immunity, adipogenesis, energy metabolism and bone mass maintenance. Due to the fact that there was a high structural similarity between GPR1 and CMKLR1，chemerin/ GPR1 signaling had similar functionality in such progresses, and to date, we already had some information about upstream and downstream molecular regulation of both signaling pathways. However, in vitro studies showed no detectable downstream signaling with binding of chemerin and CCRL2. Researches on osteoporosis mainly focused on molecular events and regulation of CMKLR1 signaling with binding of chemerin. Chemerin/CMKLR1 signaling promoted adipogenesis and inhibited osteogenesis of bone mesenchymal stem cells (BMSC), and stimulated osteoclastogenesis of hematopoietic stem cells (HSC), therefore influence bone remodeling and induce osteoporosis. Interference on this signaling could modulate differentiation of BMSC to increase bone formation and inhibit the osteoblast-independent induction of osteoclastogenesis to decrease bone resorption, thus to have potential in osteoporosis treatment. |