Abstract

Deaths of non-cardiac causes in patients with heart failure (HF) are on the rise, including lung cancer (LC). However, the common mechanisms behind the two diseases need to be further explored. This study aimed to improve understanding on the co-occurrence of LC and HF. In this study, gene expression profiles of HF (GSE57338) and LC (GSE151101) were comprehensively analyzed using the Gene Expression Omnibus database. Functional annotation, protein-protein interaction network, hub gene identification, and co-expression analysis were proceeded when the co-differentially expressed genes in HF and LC were identified. Among 44 common differentially expressed genes, 17 hub genes were identified to be associated with the co-occurrence of LC and HF; the hub genes were verified in 2 other data sets. Nine genes, including ALOX5, FPR1, ADAMTS15, ALOX5AP, ANPEP, SULF1, C1orf162, VSIG4, and LYVE1 were selected after screening. Functional analysis was performed with particular emphasis on extracellular matrix organization and regulation of leukocyte activation. Our findings suggest that disorders of the immune system could cause the co-occurrence of HF and LC. They also suggest that abnormal activation of extracellular matrix organization, inflammatory response, and other immune signaling pathways are essential in disorders of the immune system. The validated genes provide new perspectives on the common underlying pathophysiology of HF and LC, and may aid further investigation in this field.

Full Text
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