期刊
PLOS COMPUTATIONAL BIOLOGY
卷 7, 期 9, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pcbi.1002129
关键词
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资金
- European Commission [LSHG-CT-2006-037939]
- Fundacio Marato TV3-042010 Fondo de Investigaciones Sanitarias [FIS-PI061510]
- CIBERES [CB-06/06]
- ISCIII-RTICC [RD06/0020/0046]
- Comissionat per a Universitats i Recerca de la Generalitat de Catalunya [2009SGR1308, 2009SGR911]
- Spanish Government Ministry of Science and Innovation
- European Union [SAF2008-00164]
Chronic Obstructive Pulmonary Disease (COPD) is an inflammatory process of the lung inducing persistent airflow limitation. Extensive systemic effects, such as skeletal muscle dysfunction, often characterize these patients and severely limit life expectancy. Despite considerable research efforts, the molecular basis of muscle degeneration in COPD is still a matter of intense debate. In this study, we have applied a network biology approach to model the relationship between muscle molecular and physiological response to training and systemic inflammatory mediators. Our model shows that failure to coordinately activate expression of several tissue remodelling and bioenergetics pathways is a specific landmark of COPD diseased muscles. Our findings also suggest that this phenomenon may be linked to an abnormal expression of a number of histone modifiers, which we discovered correlate with oxygen utilization. These observations raised the interesting possibility that cell hypoxia may be a key factor driving skeletal muscle degeneration in COPD patients.
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