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. Author manuscript; available in PMC: 2022 Jun 1.
Published in final edited form as: Stroke. 2021 May 5;52(6):e244–e249. doi: 10.1161/STROKEAHA.121.034363

Figure 3. RBC-vascular endothelium interaction is altered by amylin deposition on RBCs and microvasculature, and is reversed by endothelial cell-secreted epoxyeicosatrienoic acids (EETs).

Figure 3

(adapted from Ref. 26). Amylin deposition on RBCs activates HIF-mediated hypoxia signaling pathways in kidneys and downstream upregulation of erythropoietin (EPO). These cellular processes are associated with pathologic erythropoiesis and arginase dysregulation within vascular tissue. EETs reduce this effect by downregulation of adhesion proteins in the vascular endothelium.