ArticleCommunications biology2023
Atsttrin regulates osteoblastogenesis and osteoclastogenesis through the TNFR pathway.
Article in Communications biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Review
- Apoptotic extracellular vesicles act as master regulators of the bone healing niche.Journal of nanobiotechnology · 2026Review
- Nanoparticles coated with osteoblast-like cell membranes as curcumin delivery vehicles for targeted postmenopausal osteoporosis therapy.Materials today. Bio · 2026Article
- Dabigatran Attenuates Osteoporosis by Balancing Osteoblastogenesis and Osteoclastogenesis by Targeting PRKAB1 and RELA.Research (Washington, D.C.) · 2026Article
- KIAA1429-mediated MCellular & molecular biology letters · 2025Article
- TNFα Receptor 1 and Not Receptor 2 Affect Annulus Fibrosus and Nucleus Pulposus Response to Cytokine Challenge in a Rat Model.JOR spine · 2025Article
- Polymethoxyflavones and Bone Metabolism.Nutrients · 2025Review
- Osteoclast Activation and Inflammatory Bone Diseases: Focusing on Receptors in Osteoclasts.Journal of inflammation research · 2025Review
- Molecular mechanisms and targeted therapy of progranulin in metabolic diseases.Frontiers in endocrinology · 2025Review
- Mediating role of inflammatory markers in the relationship between cotinine levels and total bone mineral density.PloS one · 2025Article
- Promotion of Bone Formation in a Rat Osteoporotic Vertebral Body Defect Model via Suppression of Osteoclastogenesis by Ectopic Embryonic Calvaria Derived Mesenchymal Stem Cells.International journal of molecular sciences · 2024Article
Corrections and comments
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Authors and funding
10 authors.
Funding
Abstract
Osteoporosis is a systemic metabolic bone disorder for which inflammatory cytokines play an important role. To develop new osteoporosis treatments, strategies for improving the microenvironment for osteoblast and osteoclast balance are needed. Tumor necrosis factor-α (TNF-α) plays an important role in the initiation and development of osteoporosis. Atsttrin is an engineered protein derived from the growth factor, progranulin (PGRN). The present study investigates whether Atsttrin affects osteoclast formation and osteoblast formation. Here we show Atsttrin inhibits TNF-α-induced osteoclastogenesis and inflammation. Further mechanistic investigation indicates Atsttrin inhibits TNF-α-induced osteoclastogenesis through the TNFR1 signaling pathway. Moreover, Atsttrin rescues TNF-α-mediated inhibition of osteoblastogenesis via the TNFR1 pathway. Importantly, the present study indicates that while Atsttrin cannot directly induce osteoblastogenesis, it can significantly enhance osteoblastogenesis through TNFR2-Akt-Erk1/2 signaling. These results suggest that Atsttrin treatment could potentially be a strategy for maintaining proper bone homeostasis by regulating the osteoclast/osteoblast balance. Additionally, these results provide new insights for other bone metabolism-related diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.