Macrophage polarisation under immune regulation as a therapeutic target for tendon-bone healing: multifactorial regulation and mechanistic insights

TL;DR

This paper explores how guiding macrophage polarization, especially to the anti-inflammatory M2 type, can improve healing at the tendon-bone interface.

Contribution

The paper provides mechanistic insights into how biomaterials can modulate macrophage polarization to enhance tendon-bone healing.

Findings

M2 macrophage polarization is crucial for long-term tendon-bone healing.

Biomaterials can influence macrophage behavior through multiple signaling pathways.

Controlling macrophage polarization offers new strategies for developing healing-promoting biomaterials.

Abstract

Recovery from a variety of surgical treatments, including arthroscopic rotator cuff repair and anterior cruciate ligament restoration, depends heavily on tendon-bone healing. There is mounting evidence that the polarisation of macrophages, namely M2 polarisation, is a crucial regulating factor in the repair of tendon-bone. Early tendon-bone repair is greatly aided by M1 macrophages, which have a pro-inflammatory nature. Long-term pro-inflammatory activity, however, seriously hinders the healing process. Therefore, one of the most important challenges in tendon-bone healing is to guide macrophages into the anti-inflammatory M2 phenotype. The effect of macrophage polarisation on tendon-bone healing is thoroughly investigated in this paper, along with methods for modifying macrophage polarisation. Importantly, it demonstrates how biomaterials control this process via a variety of signalling channels, providing fresh ideas for creating cutting-edge biomaterials (such as scaffolds, hydrogels, exosomes, etc.) that encourage tendon-bone mending by focusing on immune responses from macrophages.

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