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With the progression of tumors, the number of anti-tumor immune cells such as DCs, NK cells, M1 TAMs, and N1 TANs in TME decreases and their functions are suppressed while the number of immunosuppressed cells M2 TAMs, MDSCs, N2 TANs, and eTregs increases, resulting in tumor cells evading surveillance by the immune system and growing indefinitely

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Mechanistic endpoints were recorded when available, including markers of inflammation, angiogenic activity, collagen organization, and bone remodeling

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Recent injuries from weeks to months old often show faster improvement than problems persisting for years

The canonical nuclear factor kappa-B (NF-B) pathway in microglia is a critical regulator of inflammation and drives the M1 phenotype (Anilkumar and Wright-Jin, 2024)