Abstract

OBJECTIVES:Clinically, patients with chronic heart failure arising from different etiologies receive the same treatment. However, the prognoses of these patients differ. The purpose of this study was to elucidate whether the pathogenesis of heart failure arising from different etiologies differs.METHODS:Heart failure-related dataset GSE1145 was obtained from the Gene Expression Omnibus database. Differentially expressed genes were identified using R. A protein-protein interaction network of the differentially expressed genes was constructed using Search Tool for the Retrieval of Interacting Genes. The modules in each network were analyzed by Molecular Complex Detection of Cytoscape. The Database for Annotation, Visualization and Integrated Discovery was used to obtain the functions of the modules.RESULTS:Samples contained in GSE1145 were myocardial tissues from patients with dilated cardiomyopathy, familial cardiomyopathy, hypertrophic cardiomyopathy, ischemic cardiomyopathy, and post-partum cardiomyopathy. The differentially expressed genes, modules, and functions of the modules associated with different etiologies varied. Abnormal formation of extracellular matrix was overlapping among five etiologies. The change in cytoskeleton organization was specifically detected in dilated cardiomyopathy. The activation of the Wnt receptor signaling pathway was limited to hypertrophic cardiomyopathy. The change in nucleosome and chromatin assembly was associated with only familial cardiomyopathy. Germ cell migration and disrupted cellular calcium ion homeostasis were solely detected in ischemic cardiomyopathy. The change in the metabolic process of glucose and triglyceride was detected in only post-partum cardiomyopathy.CONCLUSION:These results indicate that the pathogenesis of heart failure arising from different etiologies varies, which may provide molecular evidence supporting etiology-based treatment for heart failure patients.

Highlights

  • Heart failure is the end stage of various heart diseases, including dilated cardiomyopathy, hypertension, hypertrophic cardiomyopathy, and myocardial infarction

  • The samples contained in GSE1145 were myocardial tissues from patients with heart failure arising from five different etiologies, including 12 samples arising from dilated cardiomyopathy (DCM), 5 from familial cardiomyopathy (FCM), 5 from hypertrophic cardiomyopathy (HCM), 20 from ischemic cardiomyopathy (ISCM), and 4 from post-partum cardiomyopathy (PPCM), as well as 11 normal controls

  • The number of pairs of genes included in the protein-protein interaction (PPI) networks of DCM, HCM, FCM, ISCM, and PPCM were 128, 153, 507, 719, and 160, respectively

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Summary

Introduction

Heart failure is the end stage of various heart diseases, including dilated cardiomyopathy, hypertension, hypertrophic cardiomyopathy, and myocardial infarction. Patients with heart failure suffer from a high mortality and a poor prognosis. The mortality of patients within 5 years of chronic heart failure is greater than 50% [1,2]. The incidence of heart failure has been increasing due to improvement in the treatment of underlying diseases, changes of life style, and the aging of the population [3,4,5].

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