CARDIOVASCULAR JOURNAL OF AFRICA • Volume 33, No 6, November/December 2022 AFRICA 311 dynamics when an abrupt increase in haemodynamic load is encountered. This is inferred because molecules such as cytochalasin have been previously found to inhibit changes in cell morphology, Ca2+ channel distribution and Ca2+ release, which normally occur in rat ventricular myocytes.32 Activated by mechanical stress, all three MAPKs, extracellular regulated kinases (ERKs), c-Jun NH2-terminal kinases and p38-MAPKs are included in various signalling pathways in a time-dependent manner.33 Adherens junctions act as mechanical continuity between cardiac cells; Cx43 protein is upregulated after the end of cyclic stretch, and MAPKs contribute to the enhancement of Cx43. It has also been demonstrated that ERK1/2dependent N-cadherin polarises after stretch.34 These previously characterised molecular mechanisms in response to ventricular stress provide a scientific foundation for the anti-arrhythmic effects of VRP involved in mechano-electrical feedback. Finally, we extracted hub genes from the entire PPI network to use as novel VRP targets. A total of four hub genes (Rac1, Grb2, Rbm8a and Mapk1) were identified, and most of them have been demonstrated to be correlated with the pathogenesis of mechanical overload stress. Rac1 belongs to the Rho protein family, and its activity is required for cardiomyocyte alignment, which also responds to mechanical stretch.35 Previous findings demonstrated that stretch activates and subsequently dissociates RhoA and Rac1 from caveolar compartments via the re-organisation of the actin cytoskeleton in rat cardiomyocytes.36 Franchini et al. showed that pressure overload induced a prompt activation of Grb2/Fak association (the association of the signalling molecules Grb2 and PI3 Fak kinase with Fak), which plays a central role in rat myocardium mechanotransduction after stretch.37 In addition, it has been suggested that Rbm8a plays a role in hypertension development and LV remodelling using bio-informatics analysis in patients with hypertension.38 The results of the bio-informatics analyses in our study are consistent with those of previous studies. Therefore, this study was effective in the characterisation of the anti-arrhythmic effects of VRP involved in mechano-electric feedback. Conclusion In this study, we found that VRP played a role in preventing acute mechanical change-induced ventricular arrhythmias. We used bio-informatics to analyse the anti-arrhythmic effects of VRP based on comprehensive and systematically enriched biological functions and PPI networks. GO and KEGG analyses revealed that the molecular mechanisms of VRP in preventing these ventricular arrhythmias included the pathways of adherens junctions and those involved in regulation of the actin cytoskeleton and MAPK signalling. The investigation of the module genes related to the antiarrhythmic effects of VRP may improve our understanding of the contribution of genetic factors and their interactions with the pathogenesis of mechano-electric feedback, thus aiding in the recognition of potential gene biomarkers and signalling pathways for further investigation. 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