Kupffer cells dictate hepatic responses to the atherogenic dyslipidemic insult

Di Nunzio G
March 11, 2024
Nat Cardiovasc Res
https://pubmed.ncbi.nlm.nih.gov/39196121/

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

https://pubmed.ncbi.nlm.nih.gov/39196121/

Research summary

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.

Key outcome of the study

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.

Mouse model

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.

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Keywords

Hepatology, Atherosclerosis, Dyslipidemia, Liver inflammation, Macrophage function

Technical specifications

Knockin model, Rosa26 locus, CreERT2 system, Tamoxifen-inducible gene manipulation, Conditional gene targeting

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