Work

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

Year: 2022

Type: review

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.

Source: Trends in Immunology

DOI: 10.1016/j.it.2022.09.002

Authors: Claudia Kemper, Michael N. Sack

Institutions: National Institutes of Health, National Heart, Lung, and Blood Institute

Language: English

Topic: Liver Disease Diagnosis and Treatment

Subfield: Epidemiology

Field: Medicine

Domain: Health Sciences

SDG: Good health and well-being

Open Access status: hybrid

Estimated APC paid: $6,700