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FDX1-mediated cuproptosis promotes cholestaic liver injury exacerbated by taurocholic acid

GSE300382 Mus musculus Expression profiling by high throughput sequencing 12 samples 2026/01/14 GPL24247
Summary
As the primary route for copper elimination, cholestasis raises questions about the role of copper in cholestatic liver injury and its specific molecular mechanisms. Our findings reveal that cholestasis-induced copper overload drives liver injury via taurocholic acid (TCA) -exacerbated and FDX1-mediated cuproptosis.
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NCBI GEO page ↗ Paper (PMID 41513631) ↗ {# Names what the click gives you. "Open in finder" meant nothing to a visitor who arrived from a search engine and has never seen the tool. #} Find more mouse RNA-seq datasets →
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