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Therapeutic approaches promoting conversion of M1 macrophages to an Anti-inflammatory M2 phenotype or promotion of recruitment of M2 macrophages to the wound microenvironment can lead to the resolution of inflammation and hastened healing (Fu et al., 2020

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This, in turn, stimulates downstream signaling elements dependent on both protein kinase A (PKA) and exchange protein directly activated by cAMP (EPAC) activation, which triggers the opening of voltage-dependent calcium channels (VDCCs), resulting in insulin exocytosis [24, 25]

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