This study investigates the role of Kupffer cells, the liver-resident macrophages, in modulating hepatic responses to atherogenic dyslipidemia. The research explores how Kupffer cells influence lipid metabolism, inflammation, and the progression of liver disease under dyslipidemic conditions.
Depletion or genetic modification of Kupffer cells led to significant alterations in hepatic lipid metabolism, increased inflammation, and exacerbated liver damage in response to atherogenic dyslipidemia. These findings highlight the critical role of Kupffer cells in maintaining hepatic homeostasis and protecting against lipid-induced liver injury.
The study utilized a tamoxifen-inducible CreERT2 Knockin mouse model at the Rosa26 locus to allow conditional gene recombination. By inducing Cre activity with tamoxifen, the researchers were able to selectively manipulate genes in Kupffer cells to assess their role in liver homeostasis under dyslipidemic conditions.
Hepatology, Atherosclerosis, Dyslipidemia, Liver inflammation, Macrophage function
Knockin model, Rosa26 locus, CreERT2 system, Tamoxifen-inducible gene manipulation, Conditional gene targeting
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
Certified health status from professional breeders
