This study investigated the role of PCPE-1 in liver fibrosis and nonalcoholic steatohepatitis (NASH) progression. Using Pcolce Knockout (Pcolce^-/-) mice subjected to a choline-deficient, amino acid-defined high-fat diet (CDA HFD) for 8 weeks, researchers observed that PCPE-1 deficiency significantly reduced liver fibrosis, evidenced by decreased collagen deposition and cross-linking. However, PCPE-1 deficiency did not affect hepatic steatosis, inflammation, or liver dysfunction, indicating that while PCPE-1 contributes to fibrosis development, it does not influence the progression of NASH.
PCPE-1 deficiency leads to reduced liver fibrosis without impacting steatosis or inflammation, suggesting its specific role in collagen maturation and fibrosis development in NASH.
Global Pcolce Knockout (Pcolce^-/-) mouse model, generated by constitutive deletion of the Pcolce gene to study its role in liver fibrosis and NASH progression.
Liver fibrosis, NASH, Collagen maturation, PCPE-1, Extracellular matrix remodeling
Constitutive Knockout model, Pcolce gene deletion, CDA HFD-induced NASH model
From model design to experimental results
Tailor-made solutions adapted to scientific questions
Comprehensive dataset package
Generated with biopharma partners and in-house
Scientific follow-up and advice along the project
Collaborative approach for problem solving and development of innovative models
Breeding facilities in US and Europe
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