ArticleAging cell2009
Congenital DNA repair deficiency results in protection against renal ischemia reperfusion injury in mice.
Article in Aging cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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Who cites it
12 citing papers in PubMed, 29 citations in OpenAlex.
- Article
- Development of new method to enrich human iPSC-derived renal progenitors using cell surface markers.Scientific reports · 2018Article
- DNA repair in ischemic acute kidney injury.American journal of physiology. Renal physiology · 2017Review
- TRIP13-deficient tubular epithelial cells are susceptible to apoptosis following acute kidney injury.Scientific reports · 2017Article
- DNA damage response in nephrotoxic and ischemic kidney injury.Toxicology and applied pharmacology · 2016Review
- Increased oxidative phosphorylation in response to acute and chronic DNA damage.NPJ aging and mechanisms of disease · 2016Article
- Cell Therapy Using Human Induced Pluripotent Stem Cell-Derived Renal Progenitors Ameliorates Acute Kidney Injury in Mice.Stem cells translational medicine · 2015Article
- Aag-initiated base excision repair promotes ischemia reperfusion injury in liver, brain, and kidney.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Catheter-based induction of renal ischemia/reperfusion in swine: description of an experimental model.Physiological reports · 2014Article
- DNA damage leads to progressive replicative decline but extends the life span of long-lived mutant animals.Cell death and differentiation · 2013Article
- Cockayne syndrome group B protein prevents the accumulation of damaged mitochondria by promoting mitochondrial autophagy.The Journal of experimental medicine · 2012Article
- Disorders of nucleotide excision repair: the genetic and molecular basis of heterogeneity.Nature reviews. Genetics · 2009Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Cockayne syndrome and other segmental progerias with inborn defects in DNA repair mechanisms are thought to be due in part to hypersensitivity to endogenous oxidative DNA damage. The accelerated aging-like symptoms of this disorder include dysmyelination within the central nervous system, progressive sensineuronal hearing loss and retinal degeneration. We tested the effects of congenital nucleotide excision DNA repair deficiency on acute oxidative stress sensitivity in vivo. Surprisingly, we found mouse models of Cockayne syndrome less susceptible than wild type animals to surgically induced renal ischemia reperfusion injury, a multifactorial injury mediated in part by oxidative damage. Renal failure-related mortality was significantly reduced in Csb(-/-) mice, kidney function was improved and proliferation was significantly higher in the regenerative phase following ischemic injury. Protection from ischemic damage correlated with improved baseline glucose tolerance and insulin sensitivity and a reduced inflammatory response following injury. Protection was further associated with genetic ablation of a different Cockayne syndrome-associated gene, Csa. Our data provide the first functional in vivo evidence that congenital DNA repair deficiency can induce protection from acute stress in at least one organ. This suggests that while specific types of unrepaired endogenous DNA damage may lead to detrimental effects in certain tissues, they may at the same time elicit beneficial adaptive changes in others and thus contribute to the tissue specificity of disease symptoms.
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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.