Chronic aryl hydrocarbon receptor activity phenocopies smoking-induced skeletal muscle impairment.

ABSTRACT:

Background

Chronic obstructive pulmonary disease (COPD) patients exhibit skeletal muscle atrophy, denervation, and reduced mitochondrial oxidative capacity. Whilst chronic tobacco smoke exposure is implicated in COPD muscle impairment, the mechanisms involved are ambiguous. The aryl hydrocarbon receptor (AHR) is a ligand-activated transcription factor that activates detoxifying pathways with numerous exogenous ligands, including tobacco smoke. Whereas transient AHR activation is adaptive, chronic activation can be toxic. On this basis, we tested the hypothesis that chronic smoke-induced AHR activation causes adverse muscle impact.

Methods

We used clinical patient muscle samples, and in vitro (C2C12 myotubes) and in vivo models (mouse), to perform gene expression, mitochondri

SUBMITTER: Thome T 

PROVIDER: S-EPMC8818603 | biostudies-literature | 2022 Feb

REPOSITORIES: biostudies-literature