Physical activity protects and manages heart dysfunctions by modulating the mRNA expression profiles: A bioinformatics analysis

سال انتشار: 1400
نوع سند: مقاله کنفرانسی
زبان: انگلیسی
مشاهده: 132

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شناسه ملی سند علمی:

SSRC13_079

تاریخ نمایه سازی: 8 شهریور 1401

چکیده مقاله:

Although the effects of exercise training on body performance are elucidated for everybody, evaluating the molecular signaling pathways and various mechanisms could suggest the mechanism of physical activity on the biochemical and physiological of the body. This study focuses on physical activity s influence on heart tissue function based on artificial intelligence analysis. Here, we selected the closest dataset to our aim with browsing in the Gene Expression Omnibus (GEO) server. These data were analyzed based on the Bioconductor package, Oligo, and Limma libraries in the R programming language. Moreover, the R programming language normalized microarray data based on the RMA platform. The microarray dataset analysis detected ۹۸۰ significant genes considering P.value<.۰۵ that ۶۵۲ are upregulated and ۳۲۸ downregulated in the physical activity conditions. Furthermore, a protein-protein interaction network was constructed with considering visualize parameters such as degree=۱۰, betweenness centrality=۰.۱, and closeness centrality=۰.۳ in the Cytoscape ۳.۶.۰ software and highlighted ۵۵ genes with the highest degree and betweenness. In silico analysis revealed that these ۵۵ nodes significantly had the differential expression in biventricular tissue in physical activity. The data mining and bioinformatic analysis indicated that CASP۳ with an upregulation pattern in the heart is defined as a proapoptotic and pro-inflammatory factor that is overexpressed in exercise training acutely. Based on these results, the overexpression of CASP۳ by exercise led to increased adaptation in heart tissue s physiological levels via transient heart dysfunctions, myofibrillar damage. On the other hand, we found that CASP۳ could be a candidate target for pharmaceutical design for heart damage therapeutic.