The EMBO journalAug 24, 2026

Losing Erbin in kidney tubule cells makes mice more vulnerable to sudden kidney damage and worsens scarring

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Updated Aug 26, 2026

Abstract

Erbin levels are decreased in acute kidney injury (AKI) models and chronic kidney disease (CKD) patient samples.

Erbin is highly expressed in renal tubular cells but reduced in aging-related kidney conditions.
Mice lacking Erbin in kidney tubules show increased susceptibility to AKI and worsened renal fibrosis.
Restoring Erbin levels offers protection against AKI and CKD.
Loss of Erbin in aged kidneys is linked to worsened nephropathies.
Depletion of Erbin leads to changes in the cell cycle and promotes cellular senescence.
Erbin stabilizes a protein that helps maintain cell cycle progression, potentially mitigating kidney damage.

Simplified

Aging is a major contributor to the increasing incidence of acute kidney injury (AKI) and chronic kidney disease (CKD), however the molecular events explaining aging-related nephropathies remains elusive. Here, we found that the RAS signaling adapter protein Erbin (ErbB2-interacting protein) is abundantly expressed in renal tubular cells, but its levels are decreased in murine AKI models and human CKD patient samples. Tubule-specific deletion of Erbin rendered mice highly susceptible to acute kidney injury, and exacerbated renal fibrosis. In contrast, restoring Erbin protected against AKI and CKD. Moreover, tubular Erbin loss in the naturally-aged kidney aggravates aging-associated nephropathies. Transcriptome sequencing revealed a causal association between Erbin loss and cell-cycle alterations in tubular epithelial cells. Depleting Erbin increased the proportion of tubular cells in G2/M phase and accelerated cellular senescence in vitro and in vivo. Mechanistically, Erbin protects tubular cells from senescence by stabilizing YB-1, which maintains CDK1 and cyclin B1 expression, and facilitates cell-cycle progression. Thus, restoring Erbin represents a potential strategy for chronic kidney disease and aging nephropathies.

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Losing Erbin in kidney tubule cells makes mice more vulnerable to sudden kidney damage and worsens scarring

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