ArticleNature communications2025
The long non-coding RNA RSDR protects against acute kidney injury in mice by interacting with hnRNPK to regulate DHODH-mediated ferroptosis.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Dual Compartmentalization of GSTA4 Suppresses Ferroptosis to Drive Antiandrogen Resistance in Prostate Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Echinacoside Alleviates Cisplatin-Induced Acute Kidney Injury by Regulating Bap1 to Inhibit Ferroptosis.Biomedicines · 2026Article
- Research progress on biomarkers for acute kidney injury in children.Pediatric nephrology (Berlin, Germany) · 2026Review
- Uncovering a novel treatment strategy: sodium butyrate overcomes cisplatin resistance in the oral squamous cell carcinoma by inducing ferroptosis.Journal of experimental & clinical cancer research : CR · 2026Article
- Modulating regulated cell death: mechanistic insights into traditional Chinese medicine metabolites for ischemia/reperfusion-induced acute kidney injury.Frontiers in pharmacology · 2026Review
- MTUS2-AS1 suppression promotes DDX5 protein degradation to enhance the sensitivity of PARP inhibitors in BRCA-wild triple negative breast cancer.International journal of biological sciences · 2026Article
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11 authors.
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Abstract
Acute kidney injury (AKI) is a serious clinical condition whose underlying mechanisms remain unclear. Here we identify a long non-coding RNA, RSDR, as a critical regulator of renal protection in AKI. RSDR interacts with the RNA-binding protein hnRNPK, forming a positive feedback loop that enhances the transcription of DHODH, a key ferroptosis-suppressing gene. Mechanistically, RSDR promotes the nuclear retention of hnRNPK and facilitates epigenetic activation of DHODH, thereby limiting ferroptosis in renal tubular epithelial cells. In vivo overexpression of RSDR attenuates ferroptosis and preserves renal function in male mice during AKI. Clinically, urinary RSDR levels are significantly reduced in patients with AKI, and machine learning analysis suggests potential utility in disease detection. These findings highlight RSDR as a central regulator of ferroptosis and provide mechanistic insights into lncRNA-mediated tubular protection in AKI.
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