Polyploid tubular cells and chronic kidney disease.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 36272751.
- Also identified by DOI 10.1016/j.kint.2022.08.017.
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Abstract
Defective DNA repair drives chronic kidney disease (CKD), but mechanisms are unclear. Airik and colleagues use a genetic model of defective DNA repair mimicking karyomegalic nephritis, a form of CKD characterized by tubular epithelial cells (TEC) with large nuclei and tubulointerstitial nephritis. They show that DNA damage in TEC triggers endoreplication leading to polyploid TEC and CKD. Blocking endoreplication preserved kidney function, suggesting that DNA damage triggers CKD via TEC polyploidization, questioning the concept of G2/M-arrest.
Medical subject headings
- Nephritis, Interstitial
- Renal Insufficiency, Chronic
- Nephritis