Low-intensity stimulation drives macrophage efferocytosis via ACSL4 lipid remodeling and CCL9-CCR1 signaling for tendon-bone healing.

Authors

Juncheng Yao, Yuhao Wu, Xuan Wang, Jiexin Zhang, Yan Shao, Huabin Chen, Haiyan Zhang, Haobin Li, Jianying Pan, Yitao Zhao, Daozhang Cai, Denghui Xie, Chun Zeng

Published in

Science advances. Volume 12. Issue 28. Pages eadw6666. Jul 10, 2026. Epub Jul 10, 2026.

Abstract

The mechanisms underlying exercise rehabilitation-induced 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)-mediated lipid metabolism reprogramming. Acsl4 silencing reduced fatty acid oxidation and efferocytosis, impairing exercise rehabilitation-induced 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.

PMID:
42430473
Bibliographic data and abstract were imported from PubMed on 11 Jul 2026.

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