Model depicting the contribution of Rcan1 to plaque formation Rcan1 mediates expression of the oxLDL receptor CD36 in macrophages, thus regulating oxLDL uptake. Low uptake of oxLDL by Rcan1‐deficient macrophages results in macrophage polarization to a phenotype distinct from M1 or M2. These cells display numerous anti‐inflammatory features, including high levels of IL10 and MRC1, low levels of MCP1, pronounced phagocytosis activity and weak antigen presentation (Ag pres). However, these macrophages also show increased iNOS expression. Rcan1 ablation also decreases macrophage accumulation, likely by preventing their entrapment and/or the MCP1‐mediated recruitment of additional macrophages. The lower accumulation of macrophages in the plaque and their conversion into predominantly anti‐inflammatory cells might account for the delayed plaque progression. |
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