2024-03-28 08:30:09
The results of a new study suggest that antagonism at the aryl hydrocarbon receptor could represent a therapeutic approach to combat this symptom of COPD.
Scientists at the University of Florida have determined that exposure to tobacco smoke significantly enhances the expression of the aryl hydrocarbon receptor (AHR) in skeletal muscle. The result has been obtained both in the comparison between patients with chronic obstructive pulmonary disease (COPD) and control individuals, and in an animal model. In the latter, a 50% reduction in the level of oxidative phosphorylation of muscle mitochondria was observed, in an effect dependent on the presence of AHR. This was confirmed in mice genetically deficient in this receptor, in which the negative impact of tobacco smoke was attenuated, although only in males.
Terence Ryan, director of the study, states that the muscle pathology observed could be recapitulated in mice that express a chronically active form of the AHR in skeletal muscle, which would indicate that the activation of this receptor is at least as relevant as lung damage in muscle mitochondrial dysfunction. The researcher goes on to indicate that the toxins and xenobiotic compounds contained in tobacco smoke activate the AHR, which promotes the transcription of enzymes that degrade them. However, chronic activation can be pathological, as attested to by a previous study in which, in both human- and mouse-derived specimens, exposure to tobacco smoke induced myotube atrophy, in an AHR-dependent process. Notably, in the current study the contractile function of the muscle was not affected, Ryan concludes. M.T.T./ L.D.B. (SyM)
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