Evidence map›Paper›PMID 33953223›Full record

ArticleScientific reports2021

Network pharmacology approach to decipher signaling pathways associated with target proteins of NSAIDs against COVID-19.

Ki Kwang Oh, Md Adnan, Dong Ha Cho

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
6.0field-weighted citation impact, top 3% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Potential of Gut Microbial Metabolites in Treating Osteoporosis and Obesity: A Network Pharmacology and Bioinformatics Approach.Medical science monitor : international medical journal of experimental and clinical research · 2024
    Article
  5. Review
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  7. Article
  8. Review
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  10. Inflammation Causes Exacerbation of COVID-19: How about Skin Inflammation?International journal of molecular sciences · 2022
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
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  20. Observational
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

3 authors at 1 institution in 1 country.

Ki Kwang OhDepartment of Bio-Health Convergence, College of Biomedical Science, Kangwon National University, Chuncheon, 24341, Korea.
Md AdnanDepartment of Bio-Health Convergence, College of Biomedical Science, Kangwon National University, Chuncheon, 24341, Korea.
Dong Ha ChoDepartment of Bio-Health Convergence, College of Biomedical Science, Kangwon National University, Chuncheon, 24341, Korea. chodh@kangwon.ac.kr.
Kangwon National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Non-steroidal anti-inflammatory drugs (NSAIDs) showed promising clinical efficacy toward COVID-19 (Coronavirus disease 2019) patients as potent painkillers and anti-inflammatory agents. However, the prospective anti-COVID-19 mechanisms of NSAIDs are not evidently exposed. Therefore, we intended to decipher the most influential NSAIDs candidate(s) and its novel mechanism(s) against COVID-19 by network pharmacology. FDA (U.S. Food & Drug Administration) approved NSAIDs (19 active drugs and one prodrug) were used for this study. Target proteins related to selected NSAIDs and COVID-19 related target proteins were identified by the Similarity Ensemble Approach, Swiss Target Prediction, and PubChem databases, respectively. Venn diagram identified overlapping target proteins between NSAIDs and COVID-19 related target proteins. The interactive networking between NSAIDs and overlapping target proteins was analyzed by STRING. RStudio plotted the bubble chart of the KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway enrichment analysis of overlapping target proteins. Finally, the binding affinity of NSAIDs against target proteins was determined through molecular docking test (MDT). Geneset enrichment analysis exhibited 26 signaling pathways against COVID-19. Inhibition of proinflammatory stimuli of tissues and/or cells by inactivating the RAS signaling pathway was identified as the key anti-COVID-19 mechanism of NSAIDs. Besides, MAPK8, MAPK10, and BAD target proteins were explored as the associated target proteins of the RAS. Among twenty NSAIDs, 6MNA, Rofecoxib, and Indomethacin revealed promising binding affinity with the highest docking score against three identified target proteins, respectively. Overall, our proposed three NSAIDs (6MNA, Rofecoxib, and Indomethacin) might block the RAS by inactivating its associated target proteins, thus may alleviate excessive inflammation induced by SARS-CoV-2.

Indexed as

Anti-Inflammatory Agents, Non-SteroidalAntiviral Agentsbcl-Associated Death ProteinDrug Evaluation, PreclinicalHumansMitogen-Activated Protein Kinase 10Mitogen-Activated Protein Kinase 8Molecular Targeted TherapyProtein Interaction MapsProteinsras ProteinsSARS-CoV-2Signal TransductionAnti-Inflammatory Agents, Non-SteroidalAntiviral AgentsBAD protein, humanbcl-Associated Death ProteinMitogen-Activated Protein Kinase 10Mitogen-Activated Protein Kinase 8Proteinsras Proteins

Identifiers

PMID33953223
PMCPMC8100301
OpenAlexW3159398104

What OpenQuestion holds

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LicenceCC BY
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Registered trials

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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.