Linking nutrient sensing, mitochondrial function, and PRR immune cell signaling in liver disease

Claudia Kemper*, Michael N. Sack

*Corresponding author for this work
2 Citations (Scopus)

Abstract

Caloric overconsumption in vertebrates promotes adipose and liver fat accumulation while perturbing the gut microbiome. This triad triggers pattern recognition receptor (PRR)-mediated immune cell signaling and sterile inflammation. Moreover, immune system activation perpetuates metabolic consequences, including the progression of nonalcoholic fatty liver disease (NAFLD) to nonalcoholic hepatic steatohepatitis (NASH). Recent findings show that sensing of nutrient overabundance disrupts the activity and homeostasis of the central cellular energy-generating organelle, the mitochondrion. In parallel, whether caloric excess-initiated PRR signaling and mitochondrial perturbations are coordinated to amplify this inflammatory process in NASH progression remains in question. We hypothesize that altered mitochondrial function, classic PRR signaling, and complement activation in response to nutrient overload together play an integrated role across the immune cell landscape, leading to liver inflammation and NASH progression.

Original languageEnglish
JournalTrends in Immunology
Volume43
Issue number11
Pages (from-to)886-900
Number of pages15
ISSN1471-4906
DOIs
Publication statusPublished - 11.2022

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)

DFG Research Classification Scheme

  • 204-05 Immunology

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