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Abstract
Cardiac fibrosis (CF) greatly influences the therapeutic effects of heart diseases and remains an urgent challenge in clinical therapy. Till now, only a few methods are used to find potential anti-CF drugs effectively. This study aimed to construct a gene functional module to represent the core pathological process of CF and screen antifibrotic agents capable of decreasing the expression of the gene functional module. First, three CF marker genes Postn, Ddr2, and Pdgfra were selected to identify the corresponding highest coexpressed genes in the genome-based transcriptional profiles of human hearts. Both the marker genes and the coexpressed genes formed the CF-related gene functional module. Second, the correlation of the module with the CF process was measured in a collection of gene expression profiles of heart diseases to evaluate the participation of the functional module in heart diseases. Third, the anti-CF effects of phillyrin were predicted by the enrichment analysis of the module in the phillyrin-induced transcriptional profile. Finally, the myocardial infarction animal model was used to validate the cardioprotective and anti-CF effects of phillyrin experimentally. The results showed that phillyrin was a novel antifibrotic agent in heart diseases.
Highlights
Abnormal remodeling of heart tissue characterized by cardiac fibrosis (CF) is the core pathological change in the development of various cardiovascular diseases to a certain stage (Travers et al, 2016)
The results of this study provided evidence for the potential of the specific functional gene modules in drug development and suggested phillyrin to be a novel antifibrotic agent in heart diseases
The present results could not elucidate the concrete mechanism underlying the anti-CF effect of phillyrin
Summary
Abnormal remodeling of heart tissue characterized by cardiac fibrosis (CF) is the core pathological change in the development of various cardiovascular diseases to a certain stage (Travers et al, 2016). Inhibiting or reversing the CF process has become one of the important ways to treat cardiovascular diseases. Two main drug development strategies are used for treating CF (Roubille et al, 2014; Gourdie et al, 2016). The development of antiinflammatory and immunoregulatory medications has a great potential for the CF treatment because the inflammatory response is an important initial factor of CF. Molecular pathways, such as the transforming growth factor-b1 (TGF-b1) pathway associated with the activation and proliferation of cardiac fibroblasts, play a driving role in pathological ventricular remodeling and can be representative targets for the CF treatment
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