ArticleNature communications2023
A renal YY1-KIM1-DR5 axis regulates the progression of acute kidney injury.
Article in Nature communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- Human biomarker navigator.iMeta · 2026Review
- Integrated Stress Response and Drug-Induced Acute Kidney Injury: Involvement of Activating ATF4-STAT1-GBP2 Signaling.Journal of the American Society of Nephrology : JASN · 2026Article
- The m5C orchestrator NSUN7 drives SPARC/HMGB1 axis-mediated inflammation to exacerbate kidney injury.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Acute kidney injury over the past decade: from definition evolution to pathogenesis insights and innovative therapeutic strategies.Cellular and molecular life sciences : CMLS · 2026Review
- Pressure cycling technology-assisted data-independent acquisition proteomics reveals molecular alterations and potential therapeutic targets in minor glomerular abnormalities.Precision clinical medicine · 2026Article
- Renal-tubular-mitochondrial sequentially targeted nanoagent breaks the vicious cycle of oxidative stress and mtDNA-driven inflammation in acute kidney injury therapy.Journal of nanobiotechnology · 2026Article
- Ginsenoside Rb1 targets the NRF2-PPARγ-ACSL4 axis to inhibit PTECs ferroptosis.Chinese medicine · 2026Article
- Tumor Targeting with Peptide-Drug Conjugates: Showcasing Key Progress and Hurdles.Drug design, development and therapy · 2026Review
- Biomarker-driven risk stratification and early intervention in acute kidney injury: a comprehensive review from early warning to clinical response.Frontiers in medicine · 2026Review
- YOD1 drives acute kidney injury by deubiquitinating Bax and promoting apoptosis in tubular epithelial cells.Theranostics · 2026Article
- Gain-of-function PPM1D mutations attenuate ischemic stroke.Cell death and differentiation · 2025Article
- Implant Renal Injury-Responsive Cells to Supplement Erythropoietin and Protect Kidney Injury.MedComm · 2025Article
- Histone Demethylase UTX Suppresses Tumor Cell Proliferation by Regulating Stress Granules.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The membrane-associated ubiquitin ligases MARCH2 and MARCH3 target TIM-1 to limit Zika virus infection.Cellular & molecular immunology · 2025Article
- Injured renal cell membrane encapsulated ICG/CORM-401 for homologous targeted NIR theranostics of acute kidney injury.Journal of nanobiotechnology · 2025Article
- Targeting YY1-DR5 Axis by Pyripyropene O as a Novel Therapeutic Strategy Against Prostate Cancer: Molecular Mechanisms and In Vivo Zebrafish Validation.Marine drugs · 2025Article
- A rationally designed injury kidney targeting peptide library and its application in rescuing acute kidney injury.Science advances · 2025Article
- ISG15 Enhances the Activity of γ-Glutamate Cysteine Ligase to Suppress Apoptosis in High Fat Diet-Promoted Hepatocellular Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Angiopoietin-like protein 8 directs DNA damage responses towards apoptosis by stabilizing PARP1-DNA condensates.Cell death and differentiation · 2025Article
- High-density lipoprotein nanoparticles spontaneously target to damaged renal tubules and alleviate renal fibrosis by remodeling the fibrotic niches.Nature communications · 2025Article
Corrections and comments
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Authors and funding
18 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Acute kidney injury (AKI) exhibits high morbidity and mortality. Kidney injury molecule-1 (KIM1) is dramatically upregulated in renal tubules upon injury, and acts as a biomarker for various renal diseases. However, the exact role and underlying mechanism of KIM1 in the progression of AKI remain elusive. Herein, we report that renal tubular specific knockout of Kim1 attenuates cisplatin- or ischemia/reperfusion-induced AKI in male mice. Mechanistically, transcription factor Yin Yang 1 (YY1), which is downregulated upon AKI, binds to the promoter of KIM1 and represses its expression. Injury-induced KIM1 binds to the ECD domain of death receptor 5 (DR5), which activates DR5 and the following caspase cascade by promoting its multimerization, thus induces renal cell apoptosis and exacerbates AKI. Blocking the KIM1-DR5 interaction with rationally designed peptides exhibit reno-protective effects against AKI. Here, we reveal a YY1-KIM1-DR5 axis in the progression of AKI, which warrants future exploration as therapeutic targets.
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