In cultured human renal epithelial cells, treatment with LXs attenuated TNF-<i>α</i>-driven Egr-1 activation, and Egr-1 depletion prevented cellular responses to TGF-<i>β</i>1 and TNF-<i>α</i><b>Conclusions</b> These data demonstrate that LXs can reverse established diabetic complications and support a therapeutic paradigm to promote the resolution of inflammation.