Evidence map›Paper›PMID 33923537›Full record

ReviewCells2021

Inflammasome Activation-Induced Hypercoagulopathy: Impact on Cardiovascular Dysfunction Triggered in COVID-19 Patients.

Lealem Gedefaw, Sami Ullah, Polly H M Leung, Yin Cai, Shea-Ping Yip, Chien-Ling Huang

Open access · goldAbstract readReview
In one paragraph

Review in Cells, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 30 citations in OpenAlex.

  1. Review
  2. Article
  3. COVID-19 and cardiovascular disease in patients with chronic kidney disease.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2024
    Review
  4. Review
  5. Review
  6. Review
  7. NMR-Metabolomics in COVID-19 Research.Advances in experimental medicine and biology · 2023
    Article
  8. Review
  9. Lung Inflammasome Activation in SARS-CoV-2 Post-Mortem Biopsies.International journal of molecular sciences · 2022
    Article
  10. Article
  11. Review
  12. Review
  13. Review
  14. Review
  15. Review
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

6 authors at 1 institution in 1 country.

Lealem GedefawDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Kowloon, Hong Kong, China.
Sami UllahDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Kowloon, Hong Kong, China.
Polly H M LeungDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Kowloon, Hong Kong, China.ORCID 0000-0003-2406-4773
Yin CaiDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Kowloon, Hong Kong, China.
Shea-Ping YipDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Kowloon, Hong Kong, China.ORCID 0000-0002-2170-8185
Chien-Ling HuangDepartment of Health Technology and Informatics, The Hong Kong Polytechnic University, Kowloon, Hong Kong, China.ORCID 0000-0002-6396-5649
Hong Kong Polytechnic University · HK

Funding

Health and Medical Research Fund COVID190208
6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19) is the most devastating infectious disease in the 21st century with more than 2 million lives lost in less than a year. The activation of inflammasome in the host infected by SARS-CoV-2 is highly related to cytokine storm and hypercoagulopathy, which significantly contribute to the poor prognosis of COVID-19 patients. Even though many studies have shown the host defense mechanism induced by inflammasome against various viral infections, mechanistic interactions leading to downstream cellular responses and pathogenesis in COVID-19 remain unclear. The SARS-CoV-2 infection has been associated with numerous cardiovascular disorders including acute myocardial injury, myocarditis, arrhythmias, and venous thromboembolism. The inflammatory response triggered by the activation of NLRP3 inflammasome under certain cardiovascular conditions resulted in hyperinflammation or the modulation of angiotensin-converting enzyme 2 signaling pathways. Perturbations of several target cells and tissues have been described in inflammasome activation, including pneumocytes, macrophages, endothelial cells, and dendritic cells. The interplay between inflammasome activation and hypercoagulopathy in COVID-19 patients is an emerging area to be further addressed. Targeted therapeutics to suppress inflammasome activation may have a positive effect on the reduction of hyperinflammation-induced hypercoagulopathy and cardiovascular disorders occurring as COVID-19 complications.

Indexed as

AnimalsCardiovascular DiseasesCOVID-19HumansInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinSARS-CoV-2ThrombophiliaInflammasomesNLR Family, Pyrin Domain-Containing 3 ProteinNLRP3 protein, humancardiovascular complicationsCOVID-19hypercoagulopathyinflammationNLRP3

Identifiers

PMID33923537
PMCPMC8073302
OpenAlexW3155403497

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.