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Fig. 2 | BMC Nephrology

Fig. 2

From: Macrophage polarization in innate immune responses contributing to pathogenesis of chronic kidney disease

Fig. 2

Potential roles of ApoL1 in macrophage polarization. Based on our recent in vitro observation [60], overexpression of all APOL1 variants differentiate macrophages into an atypical M1 state with a marked increase in M1 markers CD80 (not shown), TNF, IL1β, and IL6. Renal risk variants induce additional TGF-β1 and CD204 (not shown) or CD206 (not shown) expression. Renal risk variants also increase PGE2 and TBX2 via the increased expression of COX2, leading to release of TGF-β1. These results demonstrate a role of APOL1 variants in the regulation of macrophage polarization and eicosanoid metabolism, which could promote inflammatory responses and alteration of CKD processing within the injured kidney. Abbreviations: COX2, cyclooxygenase-2; IL, interleukin; PGE2, prostaglandin E2; TBX2, thromboxane B2; TGF, Transforming growth factor; TNF, tumor necrosis factor

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