Bone remodelling articles within Nature Communications

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  • Article
    | Open Access

    Angelozzi et al. uncover key mechanisms involved in physiological and pathological bone mass remodeling by showing that SOXC transcription factors regulate the bone formation and resorption balance via critical roles in LepR+ mesenchymal stem cells.

    • Marco Angelozzi
    • , Anirudha Karvande
    •  & Véronique Lefebvre

  • Article
    | Open Access

    There is a strong need for the development of effective and safe disease-modifying osteoarthritis drugs. Here, the authors show that 5-ASA, an anti-inflammatory drug used for ulcerative colitis, shows promise in treating osteoarthritis in mice by improving cartilage and reducing inflammation even when administered at late stages of disease.

    • Jihee Kim
    • , Gina Ryu
    •  & Soo Young Lee

  • Article
    | Open Access

    The TAM family of receptor tyrosine kinases exerts pleiotropic functions in health and disease. Here, the authors show that TAM receptors control osteoblastic bone formation and identified MERTK as a novel target for bone anabolic therapy and mitigation of bone metastasis including its associated osteolytic bone disease

    • Janik Engelmann
    • , Jennifer Zarrer
    •  & Sonja Loges

  • Article
    | Open Access

    The molecular circuitry that drives dendrite formation during osteocytogenesis remains poorly understood. Here the authors show that deletion of Sp7, a gene linked to rare and common skeletal disease, in mature osteoblasts and osteocytes causes severe defects in osteocyte dendrites.

    • Jialiang S. Wang
    • , Tushar Kamath
    •  & Marc N. Wein

  • Article
    | Open Access

    LncRNAs are implicated in the pathogenesis of a number of diseases. Here, the authors show that the lncRNA Nron suppresses bone resorption, and show that delivery of a functional motif of Nron increases bone mass in mouse models of osteoporosis.

    • Fujun Jin
    • , Junhui Li
    •  & Xiaogang Wang

  • Article
    | Open Access

    Osteocytes are mechanoresponsive within skeletal tissue. Here, the authors show that class IIa histone deacetylases are phosphorylated by focal adhesion kinase, suggesting that HDAC5 may propagate mechanobiological cues to regulate cell type-specific gene expression.

    • Tadatoshi Sato
    • , Shiv Verma
    •  & Marc N. Wein

  • Article
    | Open Access

    Mutations in human PIEZO2, encoding for a mechanosensitive ion channel, lead to skeletal abnormalities including scoliosis and hip dysplasia. Here, the authors show that deletion of Piezo2 in proprioceptive neurons, but not in skeletal lineages, recapitulated the human phenotype in mice.

    • Eran Assaraf
    • , Ronen Blecher
    •  & Elazar Zelzer

  • Article
    | Open Access

    Bone marrow stromal cells (BMSCs) lining sinusoidal blood vessels are mesenchymal cells whose function is critical for the skeleton. Here the authors show that quiescent CXCL12-expressing BMSCs can convert into a skeletal stem cell-like state, and differentiate into cortical bone osteoblasts only in response to injury.

    • Yuki Matsushita
    • , Mizuki Nagata
    •  & Noriaki Ono

  • Article
    | Open Access

    Mechanical forces induce bone remodeling, but how bone cells sense mechanical signaling is unclear. Here, the authors show that loss of the mechanotransduction channel Piezo1 in osteoblastic cells impairs osteoclast activity via YAP signaling and collagen expression, leading to reduced bone mass and spontaneous fractures.

    • Lijun Wang
    • , Xiuling You
    •  & Weiguo Zou

  • Article
    | Open Access

    BMP promotes bone formation but its efficacy is limited in some patients. Here, the authors show that osteoporosis patients with a poor response to BMP have increased expression of Smurf1, which targets BMP effectors for degradation, and demonstrate that its chemical inhibition enhances BMP-mediated bone formation in mice.

    • Chao Liang
    • , Songlin Peng
    •  & Ge Zhang

  • Article |

    Mechanical strain causes bone remodelling when it exceeds threshold levels of a proposed ‘lazy zone’, in which bone density is unresponsive to mechanical strain. Here the authors show that human bone remodeling is entirely load-driven, suggesting that no such ‘lazy’ state exists for human bones.

    • Patrik Christen
    • , Keita Ito
    •  & Bert van Rietbergen

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