| Literature DB >> 26250499 |
Rosa Faner1, Alba Gutiérrez-Sacristán2, Ady Castro-Acosta3, Solène Grosdidier4, Wenqi Gan5, Milagros Sánchez-Mayor4, Jose Luis Lopez-Campos6, Francisco Pozo-Rodriguez3, Ferran Sanz4, David Mannino5, Laura I Furlong4, Alvar Agusti7.
Abstract
The frequent occurrence of comorbidities in patients with chronic obstructive pulmonary disease (COPD) suggests that they may share pathobiological processes and/or risk factors.To explore these possibilities we compared the clinical diseasome and the molecular diseasome of 5447 COPD patients hospitalised because of an exacerbation of the disease. The clinical diseasome is a network representation of the relationships between diseases, in which diseases are connected if they co-occur more than expected at random; in the molecular diseasome, diseases are linked if they share associated genes or interaction between proteins.The results showed that about half of the disease pairs identified in the clinical diseasome had a biological counterpart in the molecular diseasome, particularly those related to inflammation and vascular tone regulation. Interestingly, the clinical diseasome of these patients appears independent of age, cumulative smoking exposure or severity of airflow limitation.These results support the existence of shared molecular mechanisms among comorbidities in COPD.Entities:
Mesh:
Year: 2015 PMID: 26250499 DOI: 10.1183/13993003.00763-2015
Source DB: PubMed Journal: Eur Respir J ISSN: 0903-1936 Impact factor: 16.671