Osteoporosis

Osteoporosis is a metabolic bone disorder characterized by progressive decline of bone mass and bone quality, leading to bone fragility and an increased risk of fracture. Osteoporosis occurs when bone resorption outpaces bone formation during bone remodelling.

Latest Research and Reviews

  • Research | | open

    Increased inflammation during ageing promotes osteoporosis by activating osteoclast function and inhibiting osteoblasts. Here, the authors show that TGFβ1 release from bone matrix during ageing induces degradation of TRAF3 in mesenchymal progenitor cells, leading to reduced osteoblast differentiation and increased osteoclast formation, and suggesting that pharmacological stabilization of TRAF3 could ameliorate age-related osteoporosis.

    • Jinbo Li
    • , Akram Ayoub
    • , Yan Xiu
    • , Xiaoxiang Yin
    • , James O. Sanders
    • , Addisu Mesfin
    • , Lianping Xing
    • , Zhenqiang Yao
    •  & Brendan F. Boyce
  • Research | | open

    TMCO1 is a recently described endoplasmic reticular Ca2+ channel. Here, the authors show it is important for osteoblast function and bone formation in mice, and identify a novel pathway linking local increases in Ca2+ at the ER surface with the posttranslational modification of RUNX2.

    • Jianwei Li
    • , Caizhi Liu
    • , Yuheng Li
    • , Qiaoxia Zheng
    • , Youjia Xu
    • , Beibei Liu
    • , Weijia Sun
    • , Yuan Li
    • , Shuhui Ji
    • , Mingwei Liu
    • , Jing Zhang
    • , Dingsheng Zhao
    • , Ruikai Du
    • , Zizhong Liu
    • , Guohui Zhong
    • , Cuiwei Sun
    • , Yanqing Wang
    • , Jinping Song
    • , Shu Zhang
    • , Jun Qin
    • , Shukuan Ling
    • , Xianhua Wang
    •  & Yingxian Li
  • Research |

    Here the authors identify the long noncoding RNA lnc-ob1 as a regulator of osteoblast activity. Increased lnc-ob1 expression in osteoblasts, owing to either genetic knock-in or pharmacological delivery of a plasmid, increases bone formation and counteracts bone loss in an osteoporosis mouse model, thus suggesting that modulating lnc-ob1 expression may be therapeutically useful.

    • Yao Sun
    • , Mingxiang Cai
    • , Jiayong Zhong
    • , Li Yang
    • , Jia Xiao
    • , Fujun Jin
    • , Hui Xue
    • , Xiangning Liu
    • , Huisheng Liu
    • , Yongbiao Zhang
    • , Dong Jiang
    • , An Hong
    • , Xunming Ji
    • , Zuolin Wang
    • , Gong Zhang
    •  & Xiaogang Wang
    Nature Metabolism 1, 485-496

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