ArticleComputers in biology and medicine2021
Unraveling the molecular crosstalk between Atherosclerosis and COVID-19 comorbidity.
Article in Computers in biology and medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 28 citations in OpenAlex.
- Transcriptional regulatory network analysis uncovers modular gene control and potential key regulators in diabetic cardiomyopathy.Frontiers in cell and developmental biology · 2026Article
- Macrophage-Driven Bidirectional Exacerbation in Psoriasis-Atherosclerosis Comorbidity: Insights From a Novel Mouse Model.Mediators of inflammation · 2026Article
- From Systemic Inflammation to Vascular Remodeling: Investigating Carotid IMT in COVID-19 Survivors.Viruses · 2025Article
- Drug Repurposing for COVID-19 by Constructing a Comorbidity Network with Central Nervous System Disorders.International journal of molecular sciences · 2024Article
- Proteomic and metabolomic profiling of plasma uncovers immune responses in patients with Long COVID-19.Frontiers in microbiology · 2024Article
- Article
- Mathematical model of aging in COVID-19.Journal of medical biochemistry · 2023Article
- Atherosclerosis and Inflammation: Insights from the Theory of General Pathological Processes.International journal of molecular sciences · 2023Review
- Atherosclerosis, Cardiovascular Disorders and COVID-19: Comorbid Pathogenesis.Diagnostics (Basel, Switzerland) · 2023Review
- Article
- Integrated analysis and exploration of potential shared gene signatures between carotid atherosclerosis and periodontitis.BMC medical genomics · 2022Article
- Deregulation of ceRNA Networks in Frontal Cortex and Choroid Plexus of Brain during SARS-CoV-2 Infection Aggravates Neurological Manifestations: An Insight from Bulk and Single-Cell Transcriptomic Analyses.Advanced biology · 2022Article
- A systems biology approach for investigating significantly expressed genes among COVID-19, hepatocellular carcinoma, and chronic hepatitis B.The Egyptian journal of medical human genetics · 2022Article
- Discovering common pathogenetic processes between COVID-19 and sepsis by bioinformatics and system biology approach.Frontiers in immunology · 2022Article
- COVID-19 and the Vasculature: Current Aspects and Long-Term Consequences.Frontiers in cell and developmental biology · 2022Review
- A Practical Strategy for Exploring the Pharmacological Mechanism of Luteolin Against COVID-19/Asthma Comorbidity: Findings of System Pharmacology and Bioinformatics Analysis.Frontiers in immunology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundCorona 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.
methodsWe 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.
resultsFrom 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.
conclusionFinally, 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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.