ArticleCellular & molecular biology letters2026
Targeting integrin αVβ3-Ptgs2-mTOR signaling rescues bone formation in osteoporosis: from molecular mechanism toward therapy.
Article in Cellular & molecular biology letters, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Integrin αVβ3 as a context‑dependent regulator of bone homeostasis: Insights into osteoporosis pathogenesis and therapeutic targeting (Review).Molecular medicine reports · 2026Review
- Piezo1, Integrins, and YAP/TAZ in Osteoporotic Mechanotransduction: Key Pathways, Crosstalk, and Therapeutic Implications.Calcified tissue international · 2026Review
- Integrin Signaling Imbalance in Periodontitis: A Stage-Dependent Link Between Inflammation, Bone Resorption and Regenerative Failure.Biomolecules · 2026Review
- Legumain Restrains Granuloma Formation by Inhibiting mTORC1/STAT1-Mediated M1 Macrophage Polarization in Sarcoidosis.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
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Authors and funding
9 authors.
Funding
Abstract
backgroundIntegrin αVβ3, a key ECM receptor, is essential for bone metabolism, yet its role in postmenopausal osteoporosis (PMOP) remains unclear. This study investigates the molecular mechanisms by which integrin αVβ3 regulates osteoblast function and bone homeostasis in PMOP.
methodsUsing clinical samples, OVX mice, and in vitro models, we analyzed integrin αVβ3 expression and its impact on osteogenesis. Clustered regularly interspaced short palindromic repeats (CRISPR)/Cas9-mediated knockout, multi-omics profiling, and protein interaction assays (Co-IP, BLI, and structural modeling) were employed to dissect the underlying pathway. An AAV9-based in vivo overexpression system was developed to evaluate therapeutic potential.
resultsIntegrin αVβ3 was downregulated in PMOP patients and OVX mice, correlating with osteoblast dysfunction and reduced bone formation. Mechanistically, integrin αVβ3 deficiency upregulated Ptgs2, which directly bound to mammalian target of rapamycin (mTOR) via a hydrogen bond between Ptgs2-Glu52 and mTOR-Ser2159, inhibiting mTOR phosphorylation. This suppression disrupted mTORC1-S6K/4EBP1 signaling, impairing osteoblast proliferation and survival. Notably, AAV9-mediated integrin αVβ3 overexpression rescued bone loss in OVX mice.
conclusionsOur findings unveil a novel integrin αVβ3–Ptgs2–mTOR axis in PMOP pathogenesis: estrogen deficiency reduces integrin αVβ3, enabling Ptgs2-mediated mTOR inhibition and osteogenic decline. This study identifies integrin αVβ3 as a potential therapeutic target to restore bone formation in osteoporosis.
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