Cell-specific Y-box binding protein-1 drives liver-kidney injury in cholestasis

Liu X
University Hospital RWTH-Aachen
June 12, 2026
Am J Physiol Renal Physiol
https://pubmed.ncbi.nlm.nih.gov/42284095/

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/42284095/

Research summary

The study investigated the role of YBX1 in cholestatic liver disease and associated kidney injury. Cell-specific deletion experiments demonstrated that YBX1 contributes to inflammatory signaling, fibrosis, and organ damage during cholestasis. Loss of YBX1 in specific cell populations attenuated liver injury, reduced fibrotic responses, and protected against secondary renal damage, identifying YBX1 as a potential therapeutic target in hepatorenal disease.

Key outcome of the study

Cell-specific loss of YBX1 reduced cholestasis-induced liver inflammation, fibrosis, and kidney injury. YBX1 was identified as a key regulator linking hepatic injury to downstream renal pathology.

Model

Ybx1^flox/flox conditional Knockout mouse crossed with cell-specific Cre driver lines — genOway-developed

TARGET:
Ybx1
Synonyms:
YB-1, Y-box binding protein 1, NSEP1, DBPA

Keywords

Cholestatic liver disease, liver fibrosis, kidney injury, hepatorenal syndrome, inflammation, translational disease modeling

Technical specifications

Ybx1^flox/flox conditional Knockout model, cell-specific Cre-mediated deletion, bile duct ligation model, fibrosis assessment, inflammatory gene expression profiling, liver and kidney histopathology, renal function analysis

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