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Linc-Pint Downregulation of Tgf-Β Signaling Pathway in Heart Arrhythmia: An in Silico Analysis Publisher



Amin A1 ; Ardakani MB2 ; Saadatakhtar M3 ; Zeinali A4 ; Ahadi S5 ; Fateh A6 ; Salehnassaj Z7 ; Dadgar F8, 9 ; Khodaparast F10
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Source: Journal of Diabetes and Metabolic Disorders Published:2025


Abstract

Heart Arrhythmias (HA) is one of the heart diseases that occurs due to heart dysfunction or contraction of myocardial cells. Long non-coding RNAs (LncRNAs) are one of the factors that play a role in the physiopathology of HA. TGF-β plays a pivotal role in the pathogenesis of HA. Recently, it has been shown that linc-PINT can play a role in regulating TGF-β expression. However, the interaction of these two molecules in HA has not been investigated in silico, so we evaluated this issue in this study. We accessed the GSE133420 (platform: GPL20795 HiSeq X Ten (Homo sapiens)) dataset containing RNA-seq data from human atrial appendage tissues from patients with atrial fibrillation (AF) and healthy controls. It deals with RNA isolates obtained from plasma samples. To identify potential binding sites for linc-PINT within the promoters of TGF-β signaling genes, we used LncRRIsearch. To further validate and supplement these predictions, we also referenced target genes from LncTar and starBase, which were then integrated into the protein-protein interaction (PPI) network. The results showed that the expression of linc-PINT was significantly decreased in patients compared to the control group (p < 0.01). On the other hand, the expression of SMAD2, SMAD3, SMAD5 and TGF-βR1 genes was significantly increased in patients compared to the control group. The expression of SMAD6 in both groups was almost equal and there was no significant relationship between them (P > 0.05). It can be said that examining the expression of TGF-β and linc-PINT can be helpful in identifying patients at high risk of HA, and by applying therapeutic strategies, clinical symptoms can be improved. © The Author(s), under exclusive licence to Tehran University of Medical Sciences 2025.
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