Using Machine Learning Methods in Identifying Genes Associated with COVID-19 in Cardiomyocytes and Cardiac Vascular Endothelial Cells

Abstract

Corona Virus Disease 2019 (COVID-19) not only causes respiratory system damage, but also imposes strain on the cardiovascular system. Vascular endothelial cells and cardiomyocytes play an important role in cardiac function. The aberrant expression of genes in vascular endothelial cells and cardiomyocytes can lead to cardiovascular diseases. In this study, we sought to explain the influence of respiratory syndrome coronavirus 2 (SARS-CoV-2) infection on the gene expression levels of vascular endothelial cells and cardiomyocytes. We designed an advanced machine learning-based workflow to analyze the gene expression profile data of vascular endothelial cells and cardiomyocytes from patients with COVID-19 and healthy controls. An incremental feature selection method with a decision tree was used in building efficient classifiers and summarizing quantitative classification genes and rules. Some key genes, such as MALAT1, MT-CO1, and CD36, were extracted, which exert important effects on cardiac function, from the gene expression matrix of 104,182 cardiomyocytes, including 12,007 cells from patients with COVID-19 and 92,175 cells from healthy controls, and 22,438 vascular endothelial cells, including 10,812 cells from patients with COVID-19 and 11,626 cells from healthy controls. The findings reported in this study may provide insights into the effect of COVID-19 on cardiac cells and further explain the pathogenesis of COVID-19, and they may facilitate the identification of potential therapeutic targets.

<strong></strong>An In-Depth Insight into Clinical, Cellular and Molecular Factors in COVID19-Associated Cardiovascular Ailments for Identifying Novel Disease Biomarkers, Drug Targets and Clinical Management Strategies

“…Cardiovascular disorders can be caused by atypical gene expression in vascular endothelial cells and cardiomyocytes, which are crucial in regulating heart function. Numerous genes were found to be differentially expressed in cardiomyocytes and vascular endothelial cells of COVID-19-infected heart patients as reported by Xu et al, including MALAT1, CD36, LARGE1, RYR2, PLCG2 (in cardiomyocytes), MALAT1, ID1, ID3, MT-CO1 and EGFL7 (in vascular endothelial cells) (87) . These genes regulate many vital functions in these cardiac cells (88)(89)(90)(91)(92)(93)(94)(95)(96)(97)(98)(99)(100)(101)(102)(103) .…”

<strong></strong>An In-Depth Insight into Clinical, Cellular and Molecular Factors in COVID19-Associated Cardiovascular Ailments for Identifying Novel Disease Biomarkers, Drug Targets and Clinical Management Strategies

“…The involvement of vascular endothelial cells and cardiomyocytes is crucial in regulating heart function, and cardiovascular disorders can arise as a result of the atypical expression of genes in vascular endothelial cells and cardiomyocytes. Xu et al have recently identified many genes that are differently expressed in cardiomyocytes and vascular endothelial cells of heart patients infected with COVID-19, including MALAT1, CD36, LARGE1, RYR2, PLCG2 (in cardiomyocytes), MALAT1, ID1, ID3, MT-CO1 and EGFL7 (in vascular endothelial cells) (87) . These genes regulate many vital functions in these cardiac cells (88)(89)(90)(91)(92)(93)(94)(95)(96)(97)(98)(99)(100)(101)(102)(103) .…”

The injured monocyte: The link to chronic critical illness and mortality following injury

“…This sustained change could result in increased thrombotic complications and atherosclerotic disease progression, akin to long COVID-19. [36][37][38][39][40] The early elevation in CD163, on the other hand, may be a compensatory and important scavenger receptor for free hemoglobin limiting tissue injury. However, significant elevations have been demonstrated in patients with severe sepsis going on to develop organ failure.…”