ArticleBiochimica et biophysica acta2014
DNA damage response in renal ischemia-reperfusion and ATP-depletion injury of renal tubular cells.
Article in Biochimica et biophysica acta, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 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
47 citing papers in PubMed, 1 synthesis or guideline pooled it, 74 citations in OpenAlex.
- Current perspectives and trends on the role of mitochondria in renal ischemia-reperfusion injury from 2005 to 2024: a bibliometric analysis and literature review.Frontiers in physiology · 2025Pooled it
- TRIM21 inhibition alleviates acute kidney injury by promoting INTS3-associated DNA damage repair.Apoptosis : an international journal on programmed cell death · 2026Article
- Organelle Crosstalk in Renal Cells: Insights from Cell Biology and Implications for AKI-to-CKD Transition.International journal of molecular sciences · 2026Review
- IFI16 is essential to linking DNA damage and ferroptosis in acute kidney injury.Cell death & disease · 2026Article
- The epithelial barrier theory proposes a comprehensive explanation for the origins of allergic and other chronic noncommunicable diseases.FEBS letters · 2025Review
- Cellular senescence in renal ischemia-reperfusion injury.Chinese medical journal · 2025Review
- Breast cancer gene-1 (BRCA1) potentiates maladaptive repair after kidney injury.The Journal of experimental medicine · 2025Article
- HUWE1-Mediated Degradation of MUTYH Facilitates DNA Damage and Mitochondrial Dysfunction to Promote Acute Kidney Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Molecular characterization of m6A RNA methylation regulators with features of immune dysregulation in IgA nephropathy.Clinical and experimental medicine · 2024Article
- IL-22 is secreted by proximal tubule cells and regulates DNA damage response and cell death in acute kidney injury.Kidney international · 2024Article
- Proximal TubularInternational journal of molecular sciences · 2023Article
- Renal, but not platelet or skin, extracellular vesicles decrease oxidative stress, enhance nascent peptide synthesis, and protect from ischemic renal injury.American journal of physiology. Renal physiology · 2023Article
- Functioning and mechanisms of PTMs in renal diseases.Frontiers in pharmacology · 2023Review
- ATP-induced cell death: a novel hypothesis for osteoporosis.Frontiers in cell and developmental biology · 2023Review
- Histone Modifications in Acute Kidney Injury.Kidney diseases (Basel, Switzerland) · 2022Review
- Article
- Persistent DNA damage underlies tubular cell polyploidization and progression to chronic kidney disease in kidneys deficient in the DNA repair protein FAN1.Kidney international · 2022Article
- 2-Mercaptoethanol protects against DNA double-strand breaks after kidney ischemia and reperfusion injury through GPX4 upregulation.Pharmacological reports : PR · 2022Article
- From AKI to CKD: Maladaptive Repair and the Underlying Mechanisms.International journal of molecular sciences · 2022Review
- Modeling injury and repair in kidney organoids reveals that homologous recombination governs tubular intrinsic repair.Science translational medicine · 2022Article
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 at 2 institutions in 2 countries.
Funding
Abstract
Renal ischemia-reperfusion leads to acute kidney injury (AKI) that is characterized pathologically by tubular damage and cell death, followed by tubular repair, atrophy and interstitial fibrosis. Recent work suggested the possible presence of DNA damage response (DDR) in AKI. However, the evidence is sketchy and the role and regulation of DDR in ischemic AKI remain elusive. In this study, we demonstrated the induction of phosphorylation of ATM, H2AX, Chk2 and p53 during renal ischemia-reperfusion in mice, suggesting DDR in kidney tissues. DDR was also induced in vitro during the recovery or "reperfusion" of renal proximal tubular cells (RPTCs) after ATP depletion. DDR in RPTCs was abrogated by supplying glucose to maintain ATP via glycolysis, indicating that the DDR depends on ATP depletion. The DDR was also suppressed by the general caspase inhibitor z-VAD and the overexpression of Bcl-2, supporting a role of apoptosis-associated DNA damage in the DDR. N-acetylcysteine (NAC), an antioxidant, suppressed the phosphorylation of ATM and p53 and, to a less extent, Chk2, but NAC increased the phosphorylation and nuclear foci formation of H2AX. Interestingly, NAC increased apoptosis, which may account for the observed H2AX activation. Ku55933, an ATM inhibitor, blocked ATM phosphorylation and ameliorated the phosphorylation of Chk2 and p53, but it increased H2AX phosphorylation and nuclear foci formation. Ku55933 also increased apoptosis in RPTCs following ATP depletion. The results suggest that DDR occurs during renal ischemia-reperfusion in vivo and ATP-depletion injury in vitro. The DDR is partially induced by apoptosis and oxidative stress-related DNA damage. ATM, as a sensor in the DDR, may play a cytoprotective role against tubular cell injury and death.
Indexed as
Identifiers
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.