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Adv."],"published-print":{"date-parts":[[2026,7,10]]},"abstract":"<jats:p>\n                    The mechanisms underlying exercise rehabilitation\u2013induced tendon-bone healing remain unclear. Using a mouse model of anterior cruciate ligament reconstruction, we found that low-intensity mechanical stimulation promoted macrophage M2 polarization, phagocytosis, and efferocytosis at the tendon-bone interface via acyl-CoA synthetase long-chain family member 4 (ACSL4)\u2013mediated lipid metabolism reprogramming.\n                    <jats:italic toggle=\"yes\">Acsl4<\/jats:italic>\n                    silencing reduced fatty acid oxidation and efferocytosis, impairing exercise rehabilitation\u2013induced tendon-bone healing. Notably, the CCL9-CCR1 axis contributed to bone marrow stromal cell homing following macrophage efferocytosis. In addition, engineered CCL9-expressing exosomes accelerated tendon-bone repair.\n                  <\/jats:p>","DOI":"10.1126\/sciadv.adw6666","type":"journal-article","created":{"date-parts":[[2026,7,10]],"date-time":"2026-07-10T17:58:37Z","timestamp":1783706317000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":2,"title":["Low-intensity stimulation drives macrophage efferocytosis via ACSL4 lipid remodeling and CCL9-CCR1 signaling for tendon-bone healing"],"prefix":"10.1126","volume":"12","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9490-4577","authenticated-orcid":true,"given":"Juncheng","family":"Yao","sequence":"first","affiliation":[{"name":"Department of Sports Medicine, Center for Orthopedic Surgery, The Third Affiliated Hospital, Southern Medical University, Guangzhou, China."},{"name":"Guangdong Provincial Key Laboratory of Bone and Joint Degeneration Diseases, Guangzhou, 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Lovric, T. Kanazawa, Y. Nakamura, R. A. Oliver, Y. Yu, W. R. Walsh, Effects of gaps induced into the ACL tendon graft on tendon-bone healing in a rodent ACL reconstruction model. 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