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This process leads to LPS+IFN-induced mitochondrial dysfunction and inhibition of the electron transport chain, intensifying the inflammatory response and impeding the transition from M1 to M2 macrophages ( In vivo experiments have shown that inhibiting NO production can improve mitochondrial function and reprogramming towards the M2 macrophage phenotype (Van den Bossche et al., 2016), underscoring the role of NO as a critical regulator of M1 macrophage activity

If future studies confirm these observations, GLP-1 agonists may also find applications in the treatment of difficult-to-heal wounds and ulcers

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