Chronic aryl hydrocarbon receptor activity impairs muscle mitochondrial function with tobacco smoking.

ABSTRACT:

Background

Accumulating evidence has demonstrated that chronic tobacco smoking directly contributes to skeletal muscle dysfunction independent of its pathological impact to the cardiorespiratory systems. The mechanisms underlying tobacco smoke toxicity in skeletal muscle are not fully resolved. In this study, the role of the aryl hydrocarbon receptor (AHR), a transcription factor known to be activated with tobacco smoke, was investigated.

Methods

AHR related gene (mRNA) expression was quantified in skeletal muscle from adult controls and patients with chronic obstructive pulmonary disease (COPD), as well as mice with and without cigarette smoke exposure. Utilizing both skeletal muscle-specific AHR knockout mice exposed to chronic repeated (5 days per week for 16 weeks) cigar

SUBMITTER: Fitzgerald LF 

PROVIDER: S-EPMC10995249 | biostudies-literature | 2024 Apr

REPOSITORIES: biostudies-literature