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. Author manuscript; available in PMC: 2016 Mar 1.
Published in final edited form as: Circulation. 2015 Oct 14;132(20):1898–1908. doi: 10.1161/CIRCULATIONAHA.115.017313

Figure 7.

Figure 7

Schematic representation of RBC-mediated processes fueling chronic inflammation in the setting of HFD. RBC dysfunction is promoted by several concomitantly acting mechanisms, both dependent on and independent of DARC on RBC surface (text in purple and black, respectively), leading to an increase in the levels of chemokines in the vasculature, enhanced EC-monocyte interactions, and heightened vascular inflammation. Dashed arrows comprising a possible amplification loop are hypothetical. DARC indicates Duffy antigen receptor for chemokines; EC, endothelial cell; HFD, high-fat diet; PS, phosphatidylserine; and RBC, red blood cell.