title: Systemic inflammation in chronic obstructive pulmonary disease and lung cancer: common driver of pulmonary cachexia?
abstract: OBJECTIVE
  In this article, a putative role of systemic inflammation as a driver of pulmonary cachexia induced by either chronic obstructive pulmonary disease or nonsmall cell lung cancer is reviewed. Gaps in current translational research approaches are discussed and alternative strategies are proposed to provide new insights.
  
  
  RESULTS
  Activation of the ubiquitin proteasome system has generally been considered a cause of pulmonary cachexia, but current animal models lack specificity and evidence is lacking in nonsmall cell lung cancer and conflicting in chronic obstructive pulmonary disease patients. Recent studies have shown activation of the autophagy-lysosome pathway in both nonsmall cell lung cancer and chronic obstructive pulmonary disease. Myonuclear loss, as a consequence of increased apoptotic events in myofibers, has been suggested in cancer-cachexia-associated muscle atrophy. Plasma transfer on myotube cultures can be used to detect early inflammatory signals in patients and presence of atrophy-inducing activity within the circulation.
  
  
  CONCLUSIONS
  Comparative clinical research between nonsmall cell lung cancer and chronic obstructive pulmonary disease in different disease stages is useful to unravel disease-specific versus common denominators of pulmonary cachexia.
authors.affiliation: Department of Respiratory Medicine, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Centre, Maastricht, The Netherlands.
authors.forename: Judith J M
authors.initials: JJ
authors.lastname: Ceelen
authors.forename: Ramon C J
authors.initials: RC
authors.lastname: Langen
authors.forename: Annemie M W J
authors.initials: AM
authors.lastname: Schols
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D000818:Animals; D001343:Autophagy; D002100:Cachexia / Q000209:etiology / Q000503:physiopathology*; D002289:Carcinoma, Non-Small-Cell Lung / Q000150:complications / Q000503:physiopathology*; D016207:Cytokines / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000378:metabolism; D008175:Lung Neoplasms / Q000150:complications / Q000503:physiopathology*; D008247:Lysosomes / Q000378:metabolism; D051379:Mice; D009133:Muscular Atrophy / Q000378:metabolism; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism; D029424:Pulmonary Disease, Chronic Obstructive / Q000150:complications / Q000503:physiopathology*; D025801:Ubiquitin / Q000378:metabolism
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D025801:Ubiquitin; D046988:Proteasome Endopeptidase Complex