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Efferocytosis of apoptotic neutrophils reprogrammed macrophage mitochondrial metabolism through mieloperoxidase-dependent UCP2, which increases proton conductance in the inner mitochondrial membrane, thereby impairing reactive oxygen species (mtROS) production in response to bacteria

S-adenosylmethionine (SAM), the methyl group donor substrate for DNMTs and HMTs, is formed in the one-carbon metabolism pathway, transformed to S-adenosylhomocysteine (SAH) during methylation, and then to homocysteine (HCys)