{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,3]],"date-time":"2026-08-03T23:56:56Z","timestamp":1785801416521,"version":"3.56.0"},"reference-count":65,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2026,6,8]],"date-time":"2026-06-08T00:00:00Z","timestamp":1780876800000},"content-version":"vor","delay-in-days":7,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,6,1]],"date-time":"2026-06-01T00:00:00Z","timestamp":1780272000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100016105","name":"Quzhou Municipal Science and Technology Bureau","doi-asserted-by":"publisher","award":["2023K107"],"award-info":[{"award-number":["2023K107"]}],"id":[{"id":"10.13039\/501100016105","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001809","name":"National Natural Science Foundation of China","doi-asserted-by":"publisher","award":["82372455"],"award-info":[{"award-number":["82372455"]}],"id":[{"id":"10.13039\/501100001809","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Aging Cell"],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Osteoporosis, a common metabolic bone disorder linked to aging, is often accompanied by muscle degeneration. Muscle\n                    <jats:italic>Bmal1<\/jats:italic>\n                    disruption in mice has been shown to affect various tissues, including the kidney, lung, and bone, indicating that the muscle molecular clock may influence the physiological homeostasis of multiple organs through systemic circulation. Despite this, the role of the muscle clock in age\u2010related osteoporosis remains unclear. In aged mice, we observed a disruption in the circadian interaction between muscle and bone. Furthermore, both\n                    <jats:italic>Bmal1<\/jats:italic>\n                    expression within muscle fibers and total BMAL1 protein levels in muscle tissue were significantly reduced. Using skeletal muscle\u2010specific\n                    <jats:italic>Bmal1<\/jats:italic>\n                    knockout mice, we observed osteoporosis\u2010related phenotypes, including decreased bone mass and disrupted trabecular microarchitecture, along with disrupted diurnal expression of inflammatory cytokines. Mechanistically, we revealed that muscle\n                    <jats:italic>Bmal1<\/jats:italic>\n                    deficiency impairs the rhythmic expression of the\n                    <jats:italic>Hmox1<\/jats:italic>\n                    and induces the upregulation of IL\u20101\u03b1 in muscle cells. The elevated circulating IL\u20101\u03b1 promotes osteoclast differentiation, ultimately reducing bone mass. Importantly, the osteoporosis\u2010related phenotype resulting from muscle\n                    <jats:italic>Bmal1<\/jats:italic>\n                    knockout or aging was alleviated by nighttime time\u2010restricted feeding (TRF), which reestablished a feeding\u2010driven diurnal variation in\n                    <jats:italic>Hmox1<\/jats:italic>\n                    expression within the muscle and reduced serum IL\u20101\u03b1 levels. This study provides new insights into the pathogenesis of osteoporosis in the aging population. Furthermore, it suggests that TRF may offer a promising therapeutic strategy for treating osteoporosis in the elderly.\n                  <\/jats:p>","DOI":"10.1111\/acel.70582","type":"journal-article","created":{"date-parts":[[2026,6,9]],"date-time":"2026-06-09T02:49:53Z","timestamp":1780973393000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Aging\u2010Related Muscle\n                    <i>Bmal1<\/i>\n                    Decline Contributes to Bone Loss in Mice via Enhancing\n                    <scp>IL<\/scp>\n                    \u20101\u03b1\u2013Mediated Osteoclastogenesis"],"prefix":"10.1111","volume":"25","author":[{"given":"Kai","family":"Huang","sequence":"first","affiliation":[{"name":"Orthopaedic Institute Wuxi Ninth People's Hospital Affiliated to Soochow University  Wuxi Jiangsu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jun","family":"Qian","sequence":"additional","affiliation":[{"name":"Division of Orthopaedics The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou People's Hospital  Quzhou Zhejiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yike","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Orthopaedics The Second Affiliated Hospital of Soochow University  Suzhou Jiangsu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6751-0377","authenticated-orcid":false,"given":"Feng","family":"Zhang","sequence":"additional","affiliation":[{"name":"Division of Orthopaedics The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou People's Hospital  Quzhou Zhejiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9826-4324","authenticated-orcid":false,"given":"Youjia","family":"Xu","sequence":"additional","affiliation":[{"name":"Department of Orthopaedics The Second Affiliated Hospital of Soochow University  Suzhou Jiangsu China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qiaocheng","family":"Zhai","sequence":"additional","affiliation":[{"name":"Division of Orthopaedics The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou People's Hospital  Quzhou Zhejiang 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