ReviewToxicology and applied pharmacology2016
DNA damage response in nephrotoxic and ischemic kidney injury.
Review in Toxicology and applied pharmacology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
49 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Pooled it
- Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition.International journal of molecular sciences · 2026Review
- AZD6738 overcomes acquired olaparib resistance in BRCA1 mutation triple-negative breast cancer through down-regulation of BRCA2 and RAD51.Scientific reports · 2026Article
- Pan-cancer analysis reveals DDIAS as a potential diagnostic biomarker, prognostic indicator, and tumor-immune correlate.Discover oncology · 2026Article
- IFI16 is essential to linking DNA damage and ferroptosis in acute kidney injury.Cell death & disease · 2026Article
- Targeting DNA Damage and Repair Pathways in Cerebral Ischemic Stroke: From Bench to Bedside.Translational stroke research · 2026Review
- Minichromosome maintenance 4 plays a key role in protecting against acute kidney injury by regulating tubular epithelial cells survival and regeneration.Journal of advanced research · 2026Article
- Erythropoiesis-Stimulating Agent Protects Against Kidney Fibrosis by Inhibiting G2/M Cell Cycle Arrest.Cells · 2025Article
- Cellular senescence in kidney diseases.Chinese medical journal · 2025Review
- Multimodal spatial transcriptomic characterization of mouse kidney injury and repair.Nature communications · 2025Article
- Targeting Endoplasmic Reticulum Stress by Natural and Chemical Compounds Ameliorates Cisplatin-Induced Nephrotoxicity: A Review.Biological trace element research · 2025Review
- HUWE1-Mediated Degradation of MUTYH Facilitates DNA Damage and Mitochondrial Dysfunction to Promote Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- In renal proximal tubular epithelial cells of the hibernator Syrian hamster, anoxia-reoxygenation-induced reactive oxygen species bursts do not trigger a DNA damage response and cellular senescence.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 2025Article
- Review
- Inhibition of HDAC8 mitigates AKI by reducing DNA damage and promoting homologous recombination repair.Journal of cellular and molecular medicine · 2024Article
- [High STING expression exacerbates renal ischemia-reperfusion injury in mice by regulating the TLR4/NF-κB/NLRP3 pathway and promoting inflammation and apoptosis].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2024Article
- IL-22 is secreted by proximal tubule cells and regulates DNA damage response and cell death in acute kidney injury.Kidney international · 2024Article
- GADD45A and GADD45B as Novel Biomarkers Associated with Chromatin Regulators in Renal Ischemia-Reperfusion Injury.International journal of molecular sciences · 2023Article
- Mesenchymal stem cells ameliorate cisplatin-induced acute kidney injury via let-7b-5p.Cell and tissue research · 2023Article
- DNA-dependent protein kinase catalytic subunit (DNA-PKcs) drives chronic kidney disease progression in male mice.Nature communications · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
DNA damage activates specific cell signaling cascades for DNA repair, cell cycle arrest, senescence, and/or cell death. Recent studies have demonstrated DNA damage response (DDR) in experimental models of acute kidney injury (AKI). In cisplatin-induced AKI or nephrotoxicity, the DDR pathway of ATR/Chk2/p53 is activated and contributes to renal tubular cell apoptosis. In ischemic AKI, DDR seems more complex and involves at least the ataxia telangiectasia mutated (ATM), a member of the phosphatidylinositol 3-kinase-related kinase (PIKK) family, and p53; however, while ATM may promote DNA repair, p53 may trigger cell death. Targeting DDR for kidney protection in AKI therefore relies on a thorough elucidation of the DDR pathways in various forms of AKI.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.