Inability of macrophages (MΦ) to switch from pro-inflammatory (M1, glycolytic) to anti-inflammatory (M2, oxidative) phenotype can lead to increased glucose transporter 1 (GLUT1)-mediated glucose metabolism, decreased fatty acid (FA) beta oxidation, increased intracellular lipid accumulation, and MΦ-to-foam cell transformation. Recent studies in the field of chronic venous leg ulcers have shown that iron-overloaded MΦ fail to switch from M1 to M2 phenotype. In this study we hypothesized that inability of iron-overloaded MΦ to switch from M1 to M2 phenotype underlies fatty degeneration of hemorrhagic myocardial infarction via MΦ lipid accumulation and their transformation into foam cells.
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