Loss of Erbin in tubular epithelial cells sensitizes mice to acute kidney injury and aggravates renal fibrosis.

Loss of Erbin in renal tubular cells increases susceptibility to AKI and worsens renal fibrosis in mice, with levels decreased in human CKD samples.

• Why it matters: Understanding molecular mechanisms underlying aging-related kidney diseases is crucial, as aging significantly contributes to AKI and CKD incidence, but these pathways remain poorly defined.
• What they did: The study used tubule-specific Erbin deletion in mice and transcriptome sequencing to investigate Erbin’s role, revealing its decrease in AKI and CKD, and its protective effects when restored.
• The result: Erbin loss accelerates cell-cycle arrest and senescence in tubular cells by destabilizing YB-1, suggesting that restoring Erbin could be a strategy to mitigate chronic kidney disease and aging-related nephropathies.