Key result
Nr4a1 promotes renal interstitial fibrosis potentially through activating p38 MAPK kinase, as evidenced by Csn-B exacerbating UUO-induced fibrosis and Nr4a1 downregulation preventing TGF-β1-induced fibrotic changes.
Why the study?
Renal interstitial fibrosis leads to end-stage renal disease, but its molecular mechanisms and the specific role of Nr4a1 remain largely unknown.
Population
UUO mice and TGF-beta1-treated HK-2 cells
Comparison
Nr4a1 agonist Cytosporone B or Nr4a1 siRNA vs controls
Design
Preclinical in vivo and in vitro mechanistic study
Authors
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Highlights Nr4a1-p38 axis in renal fibrosis models; hypothesis-generating for CKD but requires clinical validation.
Nr4a1 promotes renal interstitial fibrosis potentially through activating p38 MAPK kinase, highlighting a potential mechanism in chronic kidney disease progression.
Tao et al. (2023) studied Renal interstitial fibrosis. Cytosporone B (Csn-B) and Nr4a1 siRNA vs. Vehicle / NC siRNA was evaluated on Expression of fibrotic proteins (Fn, Col-I) and p38 MAPK phosphorylation. Nr4a1 promotes renal interstitial fibrosis potentially through activating p38 MAPK kinase, as evidenced by Csn-B exacerbating UUO-induced fibrosis and Nr4a1 downregulation preventing TGF-β1-induced fibrotic changes.
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