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.
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.
Ybx1^flox/flox conditional Knockout mouse crossed with cell-specific Cre driver lines — genOway-developed
Cholestatic liver disease, liver fibrosis, kidney injury, hepatorenal syndrome, inflammation, translational disease modeling
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
From model design to experimental results
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Models with certified health status from professional breeders in US and Europe