access icon free Petri Net modelling approach for analysing the behaviour of Wnt/ -catenin and Wnt/ Ca2+ signalling pathways in arrhythmogenic right ventricular cardiomyopathy

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited heart muscle disease that may result in arrhythmia, heart failure and sudden death. The hallmark pathological findings are progressive myocyte loss and fibro fatty replacement, with a predilection for the right ventricle. This study focuses on the adipose tissue formation in cardiomyocyte by considering the signal transduction pathways including Wnt/ -catenin and Wnt/Ca2+ regulation system. These pathways are modelled and analysed using stochastic petri nets (SPN) in order to increase our comprehension of ARVC and in turn its treatment regimen. The Wnt/ -catenin model predicts that the dysregulation or absence of Wnt signalling, inhibition of dishevelled and elevation of glycogen synthase kinase 3 along with casein kinase I are key cytotoxic events resulting in apoptosis. Moreover, the Wnt/Ca2+ SPN model demonstrates that the Bcl2 gene inhibited by c-Jun N-terminal kinase protein in the event of endoplasmic reticulum stress due to action potential and increased amount of intracellular Ca2+ which recovers the Ca2+ homeostasis by phospholipase C, this event positively regulates the Bcl2 to suppress the mitochondrial apoptosis which causes ARVC.

Inspec keywords: biochemistry; enzymes; molecular biophysics; calcium; cancer; biomembranes; tumours; cellular biophysics; Petri nets; muscle; genetics; bioelectric potentials; cardiology

Other keywords: Bcl2 gene; adipose tissue formation; heart failure; glycogen synthase kinase 3; Wnt signalling; Ca; $β-catenin model; Ca2+ signalling pathways; fibro fatty replacement; petri Net modelling approach; c-Jun N-terminal kinase protein; signal transduction pathways; ARVC; hallmark pathological findings; Ca2+ SPN model; progressive myocyte loss; stochastic petri nets; inherited heart muscle disease; arrhythmogenic right ventricular cardiomyopathy; Ca2+ regulation system; sudden death

Subjects: Patient care and treatment; Biomolecular interactions, charge transfer complexes; Physics of subcellular structures; Natural and artificial biomembranes; Patient diagnostic methods and instrumentation; Macromolecular configuration (bonds, dimensions); Physical chemistry of biomolecular solutions and condensed states; Biological transport; cellular and subcellular transmembrane physics; Interactions with radiations at the biomolecular level; Biomolecular structure, configuration, conformation, and active sites

http://iet.metastore.ingenta.com/content/journals/10.1049/iet-syb.2020.0038
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