Molecular and clinical diseasome of comorbidities in exacerbated COPD patients
Molecular and clinical diseasome of comorbidities in exacerbated COPD patients
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DOI：
10.1183/13993003.00763-2015
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发表时间：
2015-10-01
影响因子：
24.3
通讯作者：
Agusti, Alvar
中科院分区：
文献类型：
--
作者：
Faner, Rosa;Gutierrez-Sacristan, Alba;Agusti, Alvar
慢性阻塞性肺疾病（COPD）患者合并症频繁发生，这表明它们可能具有共同的病理生理过程和/或风险因素。为了探究这些可能性，我们比较了5447名因疾病加重而住院的COPD患者的临床疾病组和分子疾病组。临床疾病组是疾病之间关系的一种网络呈现形式，如果两种疾病同时发生的频率高于随机预期，它们就会相互连接；在分子疾病组中，如果疾病共享相关基因或蛋白质之间的相互作用，它们就会相互关联。结果显示，在临床疾病组中确定的疾病对中约有一半在分子疾病组中有对应的生物学关联，特别是那些与炎症和血管张力调节相关的疾病对。有趣的是，这些患者的临床疾病组似乎与年龄、累积吸烟暴露量或气流受限的严重程度无关。这些结果支持COPD合并症之间存在共同的分子机制。
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.