ReviewNature reviews. Nephrology2023
Pathological consequences of DNA damage in the kidney.
Review in Nature reviews. Nephrology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
What it found
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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
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Emerging Therapeutic Potential of Fisetin for Nephrotoxicity, Kidney Injury, and Nephropathy: A Systematic Review.Current diabetes reviews · 2026Pooled it
- Nucleic acid sensing pathways in kidney disease development.Nature reviews. Nephrology · 2026Review
- TRIM21 inhibition alleviates acute kidney injury by promoting INTS3-associated DNA damage repair.Apoptosis : an international journal on programmed cell death · 2026Article
- Association between 24-h proteinuria and phenotypic age acceleration in adults with preserved kidney function: a cross-sectional study.International urology and nephrology · 2026Article
- MerTK inhibition by UNC569 triggers DNA damage and JNK/p38 MAPK cascade-driven apoptosis in pancreatic cancer.Acta biochimica et biophysica Sinica · 2026Article
- cGAS-STING pathway in innate immunity and its cell-specific role in kidney diseases.Frontiers in immunology · 2026Review
- Folic acid prevents inner hair cell degeneration via genomic stability.Cell death discovery · 2025Article
- Tulp3 quantitative alleles titrate requirements for viability, brain development, and kidney homeostasis but do not suppress Zfp423 mutations in mice.PLoS genetics · 2025Article
- Cellular senescence in kidney diseases.Chinese medical journal · 2025Review
- Article
- Internal Cancers in Solid Organ Transplant Recipients with a Post-Transplant Skin Cancer: A Cohort Study.The Journal of investigative dermatology · 2025Article
- The Potential Role of Advanced Glycation End Products in the Development of Kidney Disease.Nutrients · 2025Review
- GADD45α is a direct target of TFEB and contributes to tacrolimus-induced chronic nephrotoxicity.JCI insight · 2025Article
- Hierarchical Targeting Nanodrug with Holistic DNA Protection for Effective Treatment of Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Age- and oxidative stress-induced centrosome amplification and renal stones in Drosophila Malpighian tubules.Biology open · 2024Article
- Organoids as Sophisticated Tools for Renal Cancer Research: Extensive Applications and Promising Prospects.Cellular and molecular bioengineering · 2024Review
- Inhibition of HDAC8 mitigates AKI by reducing DNA damage and promoting homologous recombination repair.Journal of cellular and molecular medicine · 2024Article
- Pathological mechanisms of kidney disease in ageing.Nature reviews. Nephrology · 2024Review
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA lesions that evade repair can lead to mutations that drive the development of cancer, and cellular responses to DNA damage can trigger senescence and cell death, which are associated with ageing. In the kidney, DNA damage has been implicated in both acute and chronic kidney injury, and in renal cell carcinoma. The susceptibility of the kidney to chemotherapeutic agents that damage DNA is well established, but an unexpected link between kidney ciliopathies and the DNA damage response has also been reported. In addition, human genetic deficiencies in DNA repair have highlighted DNA crosslinks, DNA breaks and transcription-blocking damage as lesions that are particularly toxic to the kidney. Genetic tools in mice, as well as advances in kidney organoid and single-cell RNA sequencing technologies, have provided important insights into how specific kidney cell types respond to DNA damage. The emerging view is that in the kidney, DNA damage affects the local microenvironment by triggering a damage response and cell proliferation to replenish injured cells, as well as inducing systemic responses aimed at reducing exposure to genotoxic stress. The pathological consequences of DNA damage are therefore key to the nephrotoxicity of DNA-damaging agents and the kidney phenotypes observed in human DNA repair-deficiency disorders.
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What OpenQuestion holds
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.