Loss of the E3 ubiquitin ligase MARCHF6 alters hepatic lipid metabolism and drives spontaneous hepatosteatosis

Sachdev V
University of Amsterdam
June 1, 2026
Mol Metab
https://pubmed.ncbi.nlm.nih.gov/42082151/

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

https://pubmed.ncbi.nlm.nih.gov/42082151/

Research summary

The study investigates the role of MARCHF6 in hepatic lipid homeostasis using conditional loss of Marchf6. MARCHF6 deficiency caused spontaneous hepatic steatosis and major alterations in hepatic lipid metabolism, demonstrating an essential role for this E3 ubiquitin ligase in maintaining liver metabolic homeostasis.

Key outcome of the study

Conditional loss of Marchf6 caused spontaneous hepatosteatosis and altered hepatic lipid metabolism, supporting a central role for MARCHF6 in regulating lipid and sterol homeostasis in the liver.

Model

Conditional loss of Marchf6 caused spontaneous hepatosteatosis and altered hepatic lipid metabolism, supporting a central role for MARCHF6 in regulating lipid and sterol homeostasis in the liver.

TARGET:
Marchf6
Synonyms:
TEB4, RNF176, MARCH6, Membrane Associated Ring-CH-Type Finger 6

Keywords

Hepatosteatosis, fatty liver disease, hepatic lipid metabolism, cholesterol homeostasis, metabolic disease, ubiquitin proteasome system

Technical specifications

Marchf6^flox/flox conditional Knockout, Cre-mediated gene deletion, liver-specific gene inactivation, metabolic phenotyping, liver histology, lipid analysis, gene expression analysis

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