ArticleNature communications2019
DNA damage and transcription stress cause ATP-mediated redesign of metabolism and potentiation of anti-oxidant buffering.
Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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Who cites it
49 citing papers in PubMed, 75 citations in OpenAlex.
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- Levofloxacin enhances 5-fluorouracil efficacy in colorectal cancer by activating the DDR-TP53-mitochondrial apoptosis axis.iScience · 2026Article
- Tagln1-Cre-driven Ercc1 deficiency reveals sex-specific effects on adipose tissue in mice.Endocrinology · 2026Article
- Neprilysin mediated cleavage of phospholamban dysregulates SERCA in heart failure.bioRxiv : the preprint server for biology · 2026Article
- Article
- Disulfide-Bridged Ru Complex-Mediated Photo-Disulfidptosis for Colorectal Cancer Therapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Loss of KDM6A-mediated genomic instability and metabolic reprogramming regulates response to therapeutic perturbations in bladder cancer.Nature communications · 2026Article
- Coexistence of trapped and flow-transported nuclei enables fast pigeon post communication across multinucleated cell.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- In vitro metabolomics approaches to decipher the biochemical and cellular response to genotoxic compounds.EFSA journal. European Food Safety Authority · 2025Article
- Modulating inter-mitochondrial contacts to increase membrane potential for mitigating blue light damage.bioRxiv : the preprint server for biology · 2025Article
- Targeting the crosstalk of metabolism reprogramming and replication stress: novel strategy to combat cancer.Medical oncology (Northwood, London, England) · 2025Review
- A blood-based DNA damage signature in patients with Parkinson's disease is associated with disease progression.Nature aging · 2025Article
- Loss of genome maintenance is linked to mTOR complex 1 signaling and accelerates podocyte damage.JCI insight · 2025Article
- Correction of pathogenic mitochondrial DNA in patient-derived disease models using mitochondrial base editors.PLoS biology · 2025Article
- Imaging flow cytometry-based cellular screening elucidates pathophysiology in individuals with Variants of Uncertain Significance.Genome medicine · 2025Article
- High protein intake causes gene-length-dependent transcriptional decline, shortens lifespan and accelerates ageing in progeroid DNA repair-deficient mice.npj metabolic health and disease · 2025Article
- PFKFB3-dependent redox homeostasis and DNA repair support cell survival under EGFR-TKIs in non-small cell lung carcinoma.Cancer & metabolism · 2024Article
- The brain-body energy conservation model of aging.Nature aging · 2024Review
- The dual nature of DNA damage response in obesity and bariatric surgery-induced weight loss.Cell death & disease · 2024Article
- Time is ticking faster for long genes in aging.Trends in genetics : TIG · 2024Review
Corrections and comments
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Authors and funding
19 authors at 7 institutions in 4 countries.
Funding
Abstract
Accumulation of DNA lesions causing transcription stress is associated with natural and accelerated aging and culminates with profound metabolic alterations. Our understanding of the mechanisms governing metabolic redesign upon genomic instability, however, is highly rudimentary. Using Ercc1-defective mice and Xpg knock-out mice, we demonstrate that combined defects in transcription-coupled DNA repair (TCR) and in nucleotide excision repair (NER) directly affect bioenergetics due to declined transcription, leading to increased ATP levels. This in turn inhibits glycolysis allosterically and favors glucose rerouting through the pentose phosphate shunt, eventually enhancing production of NADPH-reducing equivalents. In NER/TCR-defective mutants, augmented NADPH is not counterbalanced by increased production of pro-oxidants and thus pentose phosphate potentiation culminates in an over-reduced redox state. Skin fibroblasts from the TCR disease Cockayne syndrome confirm results in animal models. Overall, these findings unravel a mechanism connecting DNA damage and transcriptional stress to metabolic redesign and protective antioxidant defenses.
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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.