Macrophages are central regulators of wound healing, dynamically changing their function as repair progresses—initially adopting a pro-inflammatory M1-like phenotype that clears pathogens and necrotic tissue, and later transitioning toward a reparative M2-like state that suppresses inflammation, promotes angiogenesis, and supports extracellular matrix remodeling.
When this transition is disrupted, healing fails.
Persistent M1 macrophage activity sustains inflammation, prevents granulation tissue formation, and is a defining feature of chronic non-healing wounds, while an inadequate or delayed M2 response slows tissue repair and prolongs wound closure. Conversely, if M2-dominant signaling emerges too early, inflammation may be prematurely suppressed, increasing the risk of fibrosis, abnormal remodeling, or incomplete clearance of infection.
Effective wound repair therefore depends not on eliminating inflammation, but on the precise timing and regulation of the M1-to-M2 switch, a process increasingly recognized as a therapeutic target in chronic wound management, biomaterial design, and regenerative medicine.
Macrophages do not simply respond to injury—they actively determine whether healing resolves, stalls, or becomes pathological.
References (indicative)
Ferrante, C. J., & Leibovich, S. J. (2012). Regulation of Macrophage Polarization and Wound Healing. Advances in wound care, 1(1), 10–16.
Strizova, Z., Benesova, I., Bartolini, R., Novysedlak, R., Cecrdlova, E., Foley, L. K., & Striz, I. (2023). M1/M2 macrophages and their overlaps – myth or reality?. Clinical science (London, England : 1979), 137(15), 1067–1093.
Discover more from
Subscribe to get the latest posts sent to your email.
