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The lactylation of K62 on pyruvate kinase M2 (PKM2), a crucial enzyme in glycolysis, inhibits its transition from tetramer to dimer and enhances its pyruvate kinase activity, thereby suppressing inflammatory metabolic adaptation in pro-inflammatory macrophages

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While LPS exposure alone resulted in a 59% increase in oxidized DCF (a measure of ROS) compared to control cells, pretreatment with GHK-Cu at concentrations of 1, 5, and 10 µM significantly decreased ROS production