{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,8]],"date-time":"2026-03-08T04:50:18Z","timestamp":1772945418069,"version":"3.50.1"},"reference-count":28,"publisher":"Wiley","issue":"19","license":[{"start":{"date-parts":[[2020,8,30]],"date-time":"2020-08-30T00:00:00Z","timestamp":1598745600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2020,8,30]],"date-time":"2020-08-30T00:00:00Z","timestamp":1598745600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Cellular Molecular Medi"],"published-print":{"date-parts":[[2020,10]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Bone fracture is one of the most common injuries. Despite the high regenerative capacity of bones, failure of healing still occurs to near 10% of the patients. Herein, we aim to investigate the modulatory role of neurofibromatosis type I gene (NF1) to osteogenic differentiation of bone marrow\u2013derived mesenchymal stem cells (BMSCs) and new bone formation after fracture in a rat model. We studied the\n                    <jats:italic>NF1<\/jats:italic>\n                    gene expression in normal and non\u2010union bone fracture models. Then, we evaluated how\n                    <jats:italic>NF1<\/jats:italic>\n                    overexpression modulated osteogenic differentiation of BMSCs, autophagy activity, mTORC1 signalling and osteoclastic bone resorption by qRT\u2010PCR, Western blot and immunostaining assays. Finally, we injected lentivirus\u2010\n                    <jats:italic>NF1<\/jats:italic>\n                    (Lv\u2010\n                    <jats:italic>NF1<\/jats:italic>\n                    ) to rat non\u2010union bone fracture model and analysed the bone formation process. The\n                    <jats:italic>NF1<\/jats:italic>\n                    gene expression was significantly down\u2010regulated in non\u2010union bone fracture group, indicating\n                    <jats:italic>NF1<\/jats:italic>\n                    is critical in bone healing process. In the\n                    <jats:italic>NF1<\/jats:italic>\n                    overexpressing BMSCs, autophagy activity and osteogenic differentiation were significantly enhanced. Meanwhile, the\n                    <jats:italic>NF1<\/jats:italic>\n                    overexpression inhibited mTORC1 signalling and osteoclastic bone resorption. In rat non\u2010union bone fracture model, the\n                    <jats:italic>NF1<\/jats:italic>\n                    overexpression significantly promoted bone formation during fracture healing. In summary, we proved the\n                    <jats:italic>NF1<\/jats:italic>\n                    gene is critical in non\u2010union bone healing, and\n                    <jats:italic>NF1<\/jats:italic>\n                    overexpression promoted new bone formation after fracture by enhancing autophagy and inhibiting mTORC1 signalling. Our results may provide a novel therapeutic clue of promoting bone fracture healing.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.15767","type":"journal-article","created":{"date-parts":[[2020,8,30]],"date-time":"2020-08-30T12:07:39Z","timestamp":1598789259000},"page":"11524-11534","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["The neurofibromatosis type I gene promotes autophagy via mTORC1 signalling pathway to enhance new bone formation after fracture"],"prefix":"10.1111","volume":"24","author":[{"given":"Qian","family":"Tan","sequence":"first","affiliation":[{"name":"Department of Orthopedic Surgery The Hunan Children's Hospital Changsha China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jiang\u2010Yan","family":"Wu","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery The Hunan Children's Hospital Changsha China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yao\u2010Xi","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery The Hunan Children's Hospital Changsha China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Kun","family":"Liu","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery The Hunan Children's Hospital Changsha China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jin","family":"Tang","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery The Hunan Children's Hospital Changsha China"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Wei\u2010Hua","family":"Ye","sequence":"additional","affiliation":[{"name":"Department of Orthopedic Surgery The Hunan Children's Hospital Changsha 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