ArticleJBMR plus2020
The mTORC2 Component Rictor Is Required for Load-Induced Bone Formation in Late-Stage Skeletal Cells.
Article in JBMR plus, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Methodological aspects ofJournal of musculoskeletal & neuronal interactions · 2023Pooled it
- Senolytic Treatment Improves Responsiveness to Mechanical Loading in the Skeleton of Aged Mice.International journal of molecular sciences · 2025Article
- Involvement of icaritin in the regulation of osteocyte exosomal microRNAs.Journal of orthopaedic surgery and research · 2025Article
- Loss of the auxiliary αJBMR plus · 2024Article
- L-BAIBA Synergizes with Sub-Optimal Mechanical Loading to Promote New Bone Formation.JBMR plus · 2023Article
- Look who's TORking: mTOR-mediated integration of cell status and external signals during limb development and endochondral bone growth.Frontiers in cell and developmental biology · 2023Review
- Piezo1 stimulates mitochondrial function via cAMP signaling.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022Article
- Mechanically Induced Nuclear Shuttling of β-Catenin Requires Co-transfer of Actin.Stem cells (Dayton, Ohio) · 2022Article
- Review
- New Advances in Osteocyte Mechanotransduction.Current osteoporosis reports · 2021Review
- Aging, Osteo-Sarcopenia, and Musculoskeletal Mechano-Transduction.Frontiers in rehabilitation sciences · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
Bone relies on mechanical cues to build and maintain tissue composition and architecture. Our understanding of bone cell mechanotransduction continues to evolve, with a few key signaling pathways emerging as vital. Wnt/β-catenin, for example, is essential for proper anabolic response to mechanical stimulation. One key complex that regulates β-catenin activity is the mammalian target of rapamycin complex 2 (mTORc2). mTORc2 is critical for actin cytoskeletal reorganization, an indispensable component in mechanotransduction in certain cell types. In this study, we probed the impact of the mTORc2 signaling pathway in osteocyte mechanotransduction by conditionally deleting the mTORc2 subunit Rictor in Dmp1-expressing cells of C57BL/6 mice. Conditional deletion of the Rictor was achieved using the Dmp1-Cre driver to recombine Rictor floxed alleles. Rictor mutants exhibited a decrease in skeletal properties, as measured by DXA, μCT, and mechanical testing, compared with Cre-negative floxed littermate controls. in vivo axial tibia loading conducted in adult mice revealed a deficiency in the osteogenic response to loading among Rictor mutants. Histological measurements of osteocyte morphology indicated fewer, shorter cell processes in Rictor mutants, which might explain the compromised response to mechanical stimulation. In summary, inhibition of the mTORc2 pathway in late osteoblasts/osteocytes leads to decreased bone mass and mechanically induced bone formation. © 2020 The Authors.
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Registered trials
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