NR4A1 and renal fibrosis: In this study, we showed that in both in vivo and in vitro models of renal fibrosis, Nr4a1 induction was accompanied with an increase of p38 MAPK phosphorylation, and moreover, treatment of p38 MAPK inhibitor abrogated Csn-B-induced expression of fibrotic proteins(Figs. 3D and 5E-F), suggesting that Nr4a1-mediated pro-fibrotic effect is at least potentially through activating p38 MAPK.