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• W2967384659 abstract "Management of musculoskeletal disorders such as osteoporosis and osteoarthritis are a major challenge for developed countries associated with a high socioeconomic burden given the high prevalence of these diseases and the aging population. Treatment of osteoporosis has been addressed by anabolic or antiresorptive therapies. Abaloparatide, a peptide that signals through the parathormone 1 receptor (PTH1R) has been recently added to the armamentarium of bone anabolic therapies. Selective activation of PTH1R is the key of abaloparatide success in decreasing risk of fracture and increasing bone mineral density in postmenopausal women. Use of abaloparatide might be extended to other musculoskeletal disorders. Musculoskeletal disorders represent an elevated socioeconomic burden for developed aging societies. Osteoporosis (OP) has been treated with antiresorptive therapies or with teriparatide that was until recently the only anabolic therapy. However, approval of osteoporosis treatment in postmenopausal women with abaloparatide, which is an analog of parathyroid hormone-related peptide (PTHrP), has created a new alternative for OP management. The success of this new treatment is related to differential mechanisms of activation of PTH receptor type 1 (PTH1R) by abaloparatide and PTH. Here, we address the distinguishing mechanisms of PTH1R activation; the effects of PTH1R stimulation in osteoblast, osteocytes, and chondrocytes; the differences between PTH and abaloparatide actions on PTH1R; potential safety concerns; and future perspectives about abaloparatide use in other musculoskeletal disorders. Musculoskeletal disorders represent an elevated socioeconomic burden for developed aging societies. Osteoporosis (OP) has been treated with antiresorptive therapies or with teriparatide that was until recently the only anabolic therapy. However, approval of osteoporosis treatment in postmenopausal women with abaloparatide, which is an analog of parathyroid hormone-related peptide (PTHrP), has created a new alternative for OP management. The success of this new treatment is related to differential mechanisms of activation of PTH receptor type 1 (PTH1R) by abaloparatide and PTH. Here, we address the distinguishing mechanisms of PTH1R activation; the effects of PTH1R stimulation in osteoblast, osteocytes, and chondrocytes; the differences between PTH and abaloparatide actions on PTH1R; potential safety concerns; and future perspectives about abaloparatide use in other musculoskeletal disorders. analog of PTHrP that increases significantly BMD and reduces fracture risk. therapy with compounds that increase bone mass. Currently, parathyroid hormone (teriparatide), PTHrP (abaloparatide), and an antibody to sclerostin (romosozumab). therapy with compounds that are used to increase bone strength in individuals with OP. Antiresorptive compounds have high affinity for bone hydroxyapatite, can inhibit osteoclast differentiation and function, and induce osteoclast apoptosis (e.g., bisphosphonates). family of proteins that play dual roles in PTH1R signaling regulation (increase or decrease different signaling pathways). ligand-dependent selectivity for certain signal transduction pathways in the same receptor. total amount of bone tissue in the body. amount of mineralized bone tissue in a given area. specialized connective tissue that covers and protects the ends of long bones at the joints and is a structural component of several organs that require a shock-absorbing and elastic tissue. cartilage cells that synthesize and maintain the cartilaginous matrix. endochondral ossification is one of the processes in the development of the skeletal system in which bone tissue is produced from the cartilaginous tissue. intramembranous ossification is one of the processes in the development of the skeletal system in which bone tissue is produced from mesenchymal cells. process by which bone is formed. degenerative disease in which the cartilage of the joints breaks down leading to pain, stiffness and swelling. bone cells that synthesize bone matrix. bone cells that degrade (resorb) bone matrix. cells that transduce mechanical stimulus into signals that regulate osteoblast and osteoclast functions. metabolic bone disease characterized by low bone mass, a deterioration in bone tissue microarchitecture, and an increase in the susceptibility of fractures. hormone that controls levels of calcium and phosphate in the blood and influences bone loss and growth. parathyroid hormone/parathyroid hormone-related protein receptor (PTH/PTHrP type 1 receptor) is a class B G-protein-coupled receptor that regulates skeletal development, bone turnover, and mineral ion homeostasis. type of OP resulting from estrogen deficiency in women. molecule whose main function is the activation of osteoclasts (cells involved in bone resorption) by binding to RANK. series of mechanisms to protect cells from overstimulation of a receptor by a given ligand. peptide that is structurally identical to portion 1–34 of human PTH that binds PTH1R in osteoblastic cells, inducing bone formation." @default.
• W2967384659 created "2019-08-22" @default.
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• W2967384659 date "2019-10-01" @default.
• W2967384659 modified "2023-09-30" @default.
• W2967384659 title "Handling Parathormone Receptor Type 1 in Skeletal Diseases: Realities and Expectations of Abaloparatide" @default.
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• W2967384659 doi "https://doi.org/10.1016/j.tem.2019.07.014" @default.
• W2967384659 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31409530" @default.
• W2967384659 hasPublicationYear "2019" @default.
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