ArticleScientific reports2024
Nuclear receptor 4A1 ameliorates UUO-induced renal fibrosis by inhibiting the PI3K/AKT pathway.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Regulated cell death: a multidimensional regulatory network in the pathogenesis of renal fibrosis.Apoptosis : an international journal on programmed cell death · 2026Review
- NR4A1 mediates chemotherapy‑induced senescence via the PI3K/AKT pathway in gastric cancer cells.Oncology reports · 2026Article
- The subcellular localization-dependent dual role of NR4A1 in renal fibrosis: mechanisms and therapeutic perspectives.Frontiers in pharmacology · 2026Review
- Review
- NR4A3 suppresses bladder cancer progression by modulating autophagyEuropean journal of histochemistry : EJH · 2025Article
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7 authors.
Funding
Abstract
As an ultra-early response gene, Nuclear receptor 4A1 (NR4A1) has been reported to be involved in the development of various diseases through various pathological pathways, but its specific mechanism in chronic kidney disease (CKD) is unknown currently. Our study showed that the expression of NR4A1 was reduced in unilateral ureteral obstruction (UUO) mice and it could exacerbate UUO-induced renal pathological injury when knocked down NR4A1 in UUO mice. We found that the knockdown of NR4A1 could promote angiogenesis, renal inflammation, and cell apoptosis to aggravate renal fibrosis induced by UUO. As an agonist of NR4A1, Cytosporone B (Csn-B) could inhibit the renal fibrosis by attenuating angiogenesis, renal inflammation and cell apoptosis. In addition, the PI3K/AKT pathway was activated with NR4A1 knockdown in vivo and in vitro experiments. In conclusion, our study demonstrates that NR4A1 can ameliorate renal fibrosis. Furthermore, we speculate that its underlying mechanism may be related to the activation of PI3K/AKT pathway according to our present results.
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