《Table 6.Bone diseases or dysfunctions caused by adhesion GPCR mutation or deletion》

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《The role of GPCRs in bone diseases and dysfunctions》

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PTHR is the most extensively studied GPCR in bone development and disease.The PTHR SNPs rs1531137，rs1869872，rs4683301，and rs724449 were associated with reduced human height，321–323BMD，321–324and chondrodysplasia.325–326Consistently，Pthr knockout mice had reduced body length and limbs，327–329reduced trabecular BMD and osteocyte number，delayed ossification，and reduced chondrocyte proliferation and differentiation，39，329–333with increased cortical bone thickness.39，334–335PTH is a systemic hormone that regulates calcium homeostasis and bone remodeling by activating PTHR.329，335It can activate Gs and Gq，leading to cAMP production，PKA activation and stimulation of phospholipase for PKC activation to stimulate downstream signaling events.336The 1–34 amino acid peptide of PTH（PTH （1–34）） is an anti-osteoporosis drug that functions by stimulating osteoblast proliferation，337increasing osteoblast activity，338and protecting osteoblasts from apoptosis339through direct binding to PTHR.340Interestingly，PTH（1–34）also maintains intervertebral disc homeostasis during aging，suggesting that PTH has the ability to maintain skeletal homeostasis341（Table 8）.