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showed in atherosclerosis-prone apolipoprotein E-deficient (ApoE / ) and insulin-resistant mice that lixisenatide can diminish the atherosclerosis burden by reducing the size of atheroma plaques, increasing plaque stability, and reprogramming macrophages to the anti-inflammatory M2 phenotype by enhanced activation of signal transducer and activator of transcription (STAT)3, which is a determinant for M2 macrophage differentiation

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doi: 10.1016/j.cgh.2020.08.045 44

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