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Chronic aryl hydrocarbon receptor activity impairs muscle mitochondrial function with tobacco smoking
Journal of Cachexia, Sarcopenia and Muscle ( IF 8.9 ) Pub Date : 2024-02-09 , DOI: 10.1002/jcsm.13439
Liam F. Fitzgerald 1 , Jacob Lackey 2 , Ahmad Moussa 2 , Sohan V. Shah 1 , Ana Maria Castellanos 2 , Shawn Khan 2 , Martin Schonk 1 , Trace Thome 2 , Zachary R. Salyers 2 , Nishka Jakkidi 2 , Kyoungrae Kim 2 , Qingping Yang 2 , Russell T. Hepple 1, 3 , Terence E. Ryan 2, 3, 4
Affiliation  

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.

中文翻译:

慢性芳烃受体活性因吸烟而损害肌肉线粒体功能

越来越多的证据表明,长期吸烟直接导致骨骼肌功能障碍,与其对心肺系统的病理影响无关。烟草烟雾对骨骼肌毒性的机制尚未完全解决。在这项研究中,研究了芳基碳氢化合物受体(AHR)的作用,这是一种已知会被烟草烟雾激活的转录因子。
更新日期:2024-02-09
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