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Fig. 1 | Cellular & Molecular Biology Letters

Fig. 1

From: Osteoporosis: the current status of mesenchymal stem cell-based therapy

Fig. 1

Bone homeostasis regulation by OPG/RANK/RANKL system. RANKL which secreted by activated T cells functions as an osteoclast-activating factor by binding to its receptor, RANK, which is expressed on preosteoclasts. RANKL-RANK binding induces the activation of several transcription factors in preosteoclasts and initiates several downstream signaling pathways that drive osteoclast differentiation and maturation. OPG which secreted by osteoblasts, bone marrow stromal cells, and T reg cells acts as a soluble receptor that can bind to RANKL and subsequently prevents RANKL-RANK binding. Under physiologic conditions, OPG/RANKL is in equilibrium and preserves bone homeostasis. Under osteoporotic conditions, RANKL is upregulated, which is associated with downregulation of OPG. Several proinflammatory cytokines are secreted from T helper cells (Th1/Th2/Th17) stimulating and upregulating RANKL expression and mediating osteoclast formation and activity, which are linked to increased bone resorption

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