Shows low-intensity stimulation enhances macrophage efferocytosis in mice, indicating its potential for improving tendon-bone repair.
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.
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Yao et al. (2026) studied this question.
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