Unraveling the molecular crosstalk between Atherosclerosis and COVID-19 comorbidity,Computers in Biology and Medicine

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Unraveling the molecular crosstalk between Atherosclerosis and COVID-19 comorbidity
Computers in Biology and Medicine ( IF 7.0 ) Pub Date : 2021-05-01 , DOI: 10.1016/j.compbiomed.2021.104459
Deepyaman Das ₁ , Soumita Podder ₁

Affiliation

Background

Corona virus disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus −2 (SARS-CoV-2) has created ruckus throughout the world. Growing epidemiological studies have depicted atherosclerosis as a comorbid factor of COVID-19. Though both these diseases are triggered via inflammatory rage that leads to injury of healthy tissues, the molecular linkage between them and their co-influence in causing fatality is not yet understood.

Methods

We have retrieved the data of differentially expressed genes (DEGs) for both atherosclerosis and COVID-19 from publicly available microarray and RNA-Seq datasets. We then reconstructed the protein-protein interaction networks (PPIN) for these diseases from protein-protein interaction data of corresponding DEGs. Using RegNetwork and TRRUST, we mapped the transcription factors (TFs) in atherosclerosis and their targets (TGs) in COVID-19 PPIN.

Results

From the atherosclerotic PPIN, we have identified 6 hubs (TLR2, TLR4, EGFR, SPI1, MYD88 and IRF8) as differentially expressed TFs that might control the expression of their 17 targets in COVID-19 PPIN. The important target proteins include IL1B, CCL5, ITGAM, IFIT3, CXCL1, CXCL2, CXCL3 and CXCL8. Consequent functional enrichment analysis of these TGs have depicted inflammatory responses to be overrepresented among the gene sets.

Conclusion

Finally, analyzing the DEGs in cardiomyocytes infected with SARS-CoV-2, we have concluded that MYD88 is a crucial linker of atherosclerosis and COVID-19, the co-existence of which lead to fatal outcomes. Anti-inflammatory therapy targeting MYD88 could be a potent strategy for combating this comorbidity.

中文翻译：

揭开动脉粥样硬化与 COVID-19 合并症之间的分子串扰

背景

由严重急性呼吸系统综合症冠状病毒 -2 (SARS-CoV-2) 引起的 2019 年冠状病毒病 (COVID-19) 在全世界引起了轩然大波。越来越多的流行病学研究将动脉粥样硬化描述为 COVID-19 的共病因素。尽管这两种疾病都是通过炎症愤怒引发的，导致健康组织损伤，但它们之间的分子联系以及它们导致死亡的共同影响尚不清楚。

方法

我们从公开的微阵列和 RNA-Seq 数据集中检索了动脉粥样硬化和 COVID-19 的差异表达基因 (DEG) 数据。然后，我们根据相应 DEG 的蛋白质-蛋白质相互作用数据重建了这些疾病的蛋白质-蛋白质相互作用网络（PPIN）。使用 RegNetwork 和 TRRUST，我们绘制了动脉粥样硬化中的转录因子 (TF) 及其在 COVID-19 PPIN 中的靶标 (TG)。

结果

从动脉粥样硬化 PPIN 中，我们确定了 6 个中枢（TLR2、TLR4、EGFR、SPI1、MYD88 和 IRF8）作为差异表达的 TF，可能控制其在 COVID-19 PPIN 中 17 个靶标的表达。重要的靶蛋白包括IL1B、CCL5、ITGAM、IFIT3、CXCL1、CXCL2、CXCL3和CXCL8。随后对这些 TG 进行的功能富集分析表明，炎症反应在基因组中过多。