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Figure 1 | Respiratory Research

Figure 1

From: Chronic Obstructive Pulmonary Disease, inflammation and co-morbidity – a common inflammatory phenotype?

Figure 1

Pathogenic process implicated in muscle wasting in COPD. Circulating TNF-α present in some patients with COPD binds to peripheral muscle cell receptors stimulating the production of ROS and apoptosis. In addition the receptor binding stimulates NF-κB activation, possibly enhanced by ROS. Protein loss is caused directly via increased ubiquitin activity, and indirectly via decreased MyoD expression decreasing myofibril synthesis. Protein loss is amplified by a reduction in muscle use. This is the result of a reduction in IGF-1 production (leading to a decrease in myofibril synthesis), and an increase in ubiquitin activity. TNF-α – tumour necrosis factor alpha TNFR – tumour necrosis factor receptor ROS – reactive oxygen species NF-κB – nuclear factor kappa beta Ubq – ubiquitin IGF – insulin-like growth factor

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