The apolipoprotein a-i mimetic l-4f attenuates monocyte activation and adverse cardiac remodeling after myocardial infarction

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Abstract

Excessive inflammation after myocardial infarction (MI) can promote infarct expansion and adverse left ventricular (LV) remodeling. L-4F, a mimetic peptide of apolipoprotein A-I (apoA-I), exhibits anti-inflammatory and anti-atherogenic properties; however, whether L-4F imparts beneficial effects after myocardial infarction (MI) is unknown. Here we demonstrate that L-4F suppresses the expansion of blood, splenic, and myocardial pro-inflammatory monocytes and macrophages in a mouse model of reperfused MI. Changes in immune cell profiles were accompanied by alleviation of post-MI LV remodeling and dysfunction. In vitro, L-4F also inhibited pro-inflammatory and glycolytic gene expression in macrophages. In summary, L-4F treatment prevents prolonged and excessive inflammation after MI, in part through modulation of pro-inflammatory monocytes and macrophages, and improves post-MI LV remodeling. These data suggest that L-4F could be a used as a therapeutic adjunct in humans with MI to limit inflammation and alleviate the progression to heart failure.

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Hamid, T., Ismahil, M. A., Bansal, S. S., Patel, B., Goel, M., White, C. R., … Prabhu, S. D. (2020). The apolipoprotein a-i mimetic l-4f attenuates monocyte activation and adverse cardiac remodeling after myocardial infarction. International Journal of Molecular Sciences, 21(10). https://doi.org/10.3390/ijms21103519

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