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TB-4 plays a crucial role in the protection, repair, regeneration, and remodeling of injured or damaged tissues, making it a focal point in research related to tissue healing and regeneration

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Targeting metabolic vulnerabilities in specific macrophage subsets, such as limiting ferroportin-mediated iron export in M2 TAMs or enhancing ACSL4-dependent lipid peroxidation in inflammatory TAMs, may shift the TME toward a ferroptosis-permissive state