Computational Modelling of Cardiac Electrophysiological Changes in Malarial Fever.

Atkinson, Laura L.; Basharat, Aneesha; Benson, Alan P.; Colman, Michael A.; Holden, Arun V.; Kagugube, George W.; Pervolaraki, Eleftheria

doi:10.22489/cinc.2016.315-270

Cited by 1 publication

(1 citation statement)

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“…Over the past decades numerous in silico models that resemble electrophysiological properties of cardiomyocytes have been proposed based on experimental data from different species ( Krogh-Madsen et al, 2016 ; Mayourian et al, 2018 ). These models can be used to highlight physio- and pathophysiological characteristics of ion channels and cellular compartments, as well as their intricate relationships, in order to gain a mechanistic understanding of a variety of illnesses and drug-treatments ( Pandit et al, 2003 ; Sarkar and Sobie, 2011 ; Petkova-Kirova et al, 2012 ; Atkinson et al, 2016 ; Devenyi and Sobie, 2016 ; Das et al, 2017 ; Paci et al, 2018 ; Varshneya et al, 2018 ; Gong et al, 2020 ; Sutanto et al, 2020 ). However, only few models that mimic inflammation ( Petkova-Kirova et al, 2012 ) and hyperthermia ( Atkinson et al, 2016 ) can be found in the literature, posing barriers to the modeling of COVID-19 secondary effects on cardiomyocytes.…”

Section: Modeling the “Covid-19 Cardiomyocyte” In Silicomentioning

confidence: 99%

In vitro and In silico Models to Study SARS-CoV-2 Infection: Integrating Experimental and Computational Tools to Mimic “COVID-19 Cardiomyocyte”

et al. 2021

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The rapid dissemination of SARS-CoV-2 has made COVID-19 a tremendous social, economic, and health burden. Despite the efforts to understand the virus and treat the disease, many questions remain unanswered about COVID-19 mechanisms of infection and progression. Severe Acute Respiratory Syndrome (SARS) infection can affect several organs in the body including the heart, which can result in thromboembolism, myocardial injury, acute coronary syndromes, and arrhythmias. Numerous cardiac adverse events, from cardiomyocyte death to secondary effects caused by exaggerated immunological response against the virus, have been clinically reported. In addition to the disease itself, repurposing of treatments by using “off label” drugs can also contribute to cardiotoxicity. Over the past several decades, animal models and more recently, stem cell-derived cardiomyocytes have been proposed for studying diseases and testing treatments in vitro. In addition, mechanistic in silico models have been widely used for disease and drug studies. In these models, several characteristics such as gender, electrolyte imbalance, and comorbidities can be implemented to study pathophysiology of cardiac diseases and to predict cardiotoxicity of drug treatments. In this Mini Review, we (1) present the state of the art of in vitro and in silico cardiomyocyte modeling currently in use to study COVID-19, (2) review in vitro and in silico models that can be adopted to mimic the effects of SARS-CoV-2 infection on cardiac function, and (3) provide a perspective on how to combine some of these models to mimic “COVID-19 cardiomyocytes environment.”

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