ArticleInternational journal of molecular medicine2021
Peptide 11R‑VIVIT promotes fracture healing in osteoporotic rats.
Article in International journal of molecular medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- TRP120-dependent activation of noncanonical Wnt/NFAT signaling drives monocyte chemokine production inmSphere · 2026Article
- Metformin facilitates osteogenic differentiation of bone marrow stromal cells through AMPK-dependent autophagy: an investigation into the healing of osteoporotic fractures in murine models.Journal of orthopaedic surgery and research · 2025Article
- Hydroxylated fullerene promotes fracture healing in ovariectomized combined type 2 diabetic mice.Journal of orthopaedic surgery and research · 2025Article
- Erianin serves as an NFATc1 inhibitor to prevent breast cancer-induced osteoclastogenesis and bone destruction.Journal of advanced research · 2025Article
- Estrogen deficiency impedes fracture healing despite eliminating the excessive absorption of the posterior callus in a semi-fixed distal tibial fracture mouse model.BMC musculoskeletal disorders · 2023Article
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Authors and funding
6 authors.
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Abstract
Osteoporotic fracture healing is a complex clinical issue. The present study was conducted to investigate the repair properties of 11R‑VIVIT on osteoporotic fractures and to examine the potential effects of 11R‑VIVIT on osteoporotic bone marrow‑derived mesenchymal stem cells (BMSCs), A rat model of osteoporotic femoral fracture was established, and the effects of the daily local injection of 11R‑VIVIT or saline on fracture repairing were evaluated by micro‑CT scans and H&E staining. Moreover, BMSCs from osteoporotic rats were treated with 11R‑VIVIT, and the osteogenic and adipogenic differentiation of BMSCs was evaluated. The results revealed that 11R‑VIVIT promoted bone formation and increased fracture healing. In addition, 11R‑VIVIT promoted the differentiation of osteoporotic BMSCs into osteoblasts rather than adipocytes. Furthermore, mechanistic analysis revealed that 11R‑VIVIT promoted autophagy by blocking the protein kinase B (AKT)/nuclear factor of activated T‑cells (NFATc1) signaling pathway. Consistently, the activation and inhibition of autophagy using rapamycin and LY294002 confirmed the regulatory effects of 11R‑VIVIT on autophagy. On the whole, the findings of the present study demonstrate that 11R‑VIVIT promotes fracture healing in osteoporotic rats and enhances the osteogenic differentiation of osteoporotic BMSCs by dysregulating the AKT/NFATc1 signaling pathway.
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