Unraveling the molecular crosstalk between Atherosclerosis and COVID-19 comorbidity

Das, Deepyaman; Podder, Soumita

doi:10.1016/j.compbiomed.2021.104459

Cited by 21 publications

(19 citation statements)

References 94 publications

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“…To shed more light on the impact of atherosclerosis for COVID-19 Das and Podder retrieved data of differentially expressed genes for both, atherosclerosis, and COVID-19, from publicly available microarray and RNAseq datasets and performed a protein-protein interaction network analysis. Further functional enrichment revealed inflammatory response genes to be more abundant, particularly MyD88 was identified as a crucial linker of atherosclerosis and COVID-19 ( Das and Podder, 2021 ).…”

Section: Sars-cov-2mentioning

confidence: 99%

COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences

Martínez-Salazar

Holwerda

Stüdle

et al. 2022

Front. Cell Dev. Biol.

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Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) was first identified in December 2019 as a novel respiratory pathogen and is the causative agent of Corona Virus disease 2019 (COVID-19). Early on during this pandemic, it became apparent that SARS-CoV-2 was not only restricted to infecting the respiratory tract, but the virus was also found in other tissues, including the vasculature. Individuals with underlying pre-existing co-morbidities like diabetes and hypertension have been more prone to develop severe illness and fatal outcomes during COVID-19. In addition, critical clinical observations made in COVID-19 patients include hypercoagulation, cardiomyopathy, heart arrythmia, and endothelial dysfunction, which are indicative for an involvement of the vasculature in COVID-19 pathology. Hence, this review summarizes the impact of SARS-CoV-2 infection on the vasculature and details how the virus promotes (chronic) vascular inflammation. We provide a general overview of SARS-CoV-2, its entry determinant Angiotensin-Converting Enzyme II (ACE2) and the detection of the SARS-CoV-2 in extrapulmonary tissue. Further, we describe the relation between COVID-19 and cardiovascular diseases (CVD) and their impact on the heart and vasculature. Clinical findings on endothelial changes during COVID-19 are reviewed in detail and recent evidence from in vitro studies on the susceptibility of endothelial cells to SARS-CoV-2 infection is discussed. We conclude with current notions on the contribution of cardiovascular events to long term consequences of COVID-19, also known as “Long-COVID-syndrome”. Altogether, our review provides a detailed overview of the current perspectives of COVID-19 and its influence on the vasculature.

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Section: Sars-cov-2mentioning

confidence: 99%

COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences

Martínez-Salazar

Holwerda

Stüdle

et al. 2022

Front. Cell Dev. Biol.

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“…Therefore, this study mitigates the gaps in the literature through the above mentioned contributions. It is to be noted that other works like [ 41 , 42 ] have analysed drug repurposibility and comorbidities by considering expression data as opposed to our work which directly considers PPI data for the above analysis.…”

Section: Introductionmentioning

confidence: 99%

Interactome of human and SARS-CoV-2 proteins to identify human hub proteins associated with comorbidities

Ghosh

Saha

Sharma

2021

Computers in Biology and Medicine

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SARS-CoV-2 has a higher chance of progression in adults of any age with certain underlying health conditions or comorbidities like cancer, neurological diseases and in certain cases may even lead to death. Like other viruses, SARS-CoV-2 also interacts with host proteins to pave its entry into host cells. Therefore, to understand the behaviour of SARS-CoV-2 and design of effective antiviral drugs, host-virus protein-protein interactions (PPIs) can be very useful. In this regard, we have initially created a human-SARS-CoV-2 PPI database from existing works in the literature which has resulted in 7085 unique PPIs. Subsequently, we have identified at most 10 proteins with highest degrees viz. hub proteins from interacting human proteins for individual virus protein. The identification of these hub proteins is important as they are connected to most of the other human proteins. Consequently, when they get affected, the potential diseases are triggered in the corresponding pathways, thereby leading to comorbidities. Furthermore, the biological significance of the identified hub proteins is shown using KEGG pathway and GO enrichment analysis. KEGG pathway analysis is also essential for identifying the pathways leading to comorbidities. Among others, SARS-CoV-2 proteins viz. NSP2, NSP5, Envelope and ORF10 interacting with human hub proteins like COX4I1, COX5A, COX5B, NDUFS1, CANX, HSP90AA1 and TP53 lead to comorbidities. Such comorbidities are Alzheimer, Parkinson, Huntington, HTLV-1 infection, prostate cancer and viral carcinogenesis. Subsequently, using Enrichr tool possible repurposable drugs which target the human hub proteins are reported in this paper as well. Therefore, this work provides a consolidated study for human-SARS-CoV-2 protein interactions to understand the relationship between comorbidity and hub proteins so that it may pave the way for the development of anti-viral drugs.

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“…The integrin CD11b encoded by ITGAM is expressed on the surface of macrophages and is involved in adhesion, migration and cell-mediated cytotoxicity ( 69 ). Studies have found that CD11b can mediate thrombus formation in COVID-19, so ITGAM plays an important role in thrombus formation in COVID-19 patients ( 70 ). Another study found that ITGAM also plays an important role in methicillin-resistant Staphylococcus aureus (MRSA)-induced sepsis.…”

Section: Discussionmentioning

confidence: 99%

Discovering common pathogenetic processes between COVID-19 and sepsis by bioinformatics and system biology approach

Liu

Gui

et al. 2022

Front. Immunol.

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Corona Virus Disease 2019 (COVID-19), an acute respiratory infectious disease caused by severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), has spread rapidly worldwide, resulting in a pandemic with a high mortality rate. In clinical practice, we have noted that many critically ill or critically ill patients with COVID-19 present with typical sepsis-related clinical manifestations, including multiple organ dysfunction syndrome, coagulopathy, and septic shock. In addition, it has been demonstrated that severe COVID-19 has some pathological similarities with sepsis, such as cytokine storm, hypercoagulable state after blood balance is disrupted and neutrophil dysfunction. Considering the parallels between COVID-19 and non-SARS-CoV-2 induced sepsis (hereafter referred to as sepsis), the aim of this study was to analyze the underlying molecular mechanisms between these two diseases by bioinformatics and a systems biology approach, providing new insights into the pathogenesis of COVID-19 and the development of new treatments. Specifically, the gene expression profiles of COVID-19 and sepsis patients were obtained from the Gene Expression Omnibus (GEO) database and compared to extract common differentially expressed genes (DEGs). Subsequently, common DEGs were used to investigate the genetic links between COVID-19 and sepsis. Based on enrichment analysis of common DEGs, many pathways closely related to inflammatory response were observed, such as Cytokine-cytokine receptor interaction pathway and NF-kappa B signaling pathway. In addition, protein-protein interaction networks and gene regulatory networks of common DEGs were constructed, and the analysis results showed that ITGAM may be a potential key biomarker base on regulatory analysis. Furthermore, a disease diagnostic model and risk prediction nomogram for COVID-19 were constructed using machine learning methods. Finally, potential therapeutic agents, including progesterone and emetine, were screened through drug-protein interaction networks and molecular docking simulations. We hope to provide new strategies for future research and treatment related to COVID-19 by elucidating the pathogenesis and genetic mechanisms between COVID-19 and sepsis.

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Unraveling the molecular crosstalk between Atherosclerosis and COVID-19 comorbidity

Cited by 21 publications

References 94 publications

COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences

COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences

Interactome of human and SARS-CoV-2 proteins to identify human hub proteins associated with comorbidities

Discovering common pathogenetic processes between COVID-19 and sepsis by bioinformatics and system biology approach

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