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Moreover, chronic hyperglycemia leads to increased PKC activation via increased de novo synthesis of DAG, which activates multiple PKC isoforms in diabetic platelets, particularly PKC2 and PKC (Geraldes and King, 2010), where upregulation of PKC2 has been linked to microvascular complications such as retinopathy and nephropathy, and consequent PKC inhibition and insulin treatment have been shown to reduce platelet hyperactivity (Kimura et al., 2001)

doi: 10.1001/jamapsychiatry.2019.0774