Evidence map›Paper›PMID 34769508›Full record

ReviewInternational journal of molecular sciences2021

Pathogenic Basis of Thromboinflammation and Endothelial Injury in COVID-19: Current Findings and Therapeutic Implications.

Yasutomi Higashikuni, Wenhao Liu, Takumi Obana, Masataka Sata

Open access · goldAbstract readReview
In one paragraph

Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.9field-weighted citation impact, top 12% 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

30 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Imaging of Thromboinflammation by MultispectralInternational journal of molecular sciences · 2025
    Review
  6. Article
  7. Apoptotic Vesicles Attenuate Acute Lung InjuryInternational journal of nanomedicine · 2025
    Article
  8. Review
  9. Review
  10. Illustrated State-of-the-Art Capsules of the ISTH 2024 Congress.Research and practice in thrombosis and haemostasis · 2024
    Article
  11. Article
  12. Review
  13. Article
  14. Observational
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
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

4 authors at 2 institutions in 1 country.

Yasutomi HigashikuniDepartment of Cardiovascular Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0002-2232-567X
Wenhao LiuDepartment of Cardiovascular Medicine, The University of Tokyo, Tokyo 113-8655, Japan.ORCID 0000-0002-2243-8391
Takumi ObanaDepartment of Cardiovascular Medicine, The University of Tokyo, Tokyo 113-8655, Japan.
Masataka SataDepartment of Cardiovascular Medicine, The University of Tokushima, Tokushima 770-8503, Japan.ORCID 0000-0002-8036-7501
The University of Tokyo · JPTokushima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has become a global pandemic with a great impact on social and economic activities, as well as public health. In most patients, the symptoms of COVID-19 are a high-grade fever and a dry cough, and spontaneously resolve within ten days. However, in severe cases, COVID-19 leads to atypical bilateral interstitial pneumonia, acute respiratory distress syndrome, and systemic thromboembolism, resulting in multiple organ failure with high mortality and morbidity. SARS-CoV-2 has immune evasion mechanisms, including inhibition of interferon signaling and suppression of T cell and B cell responses. SARS-CoV-2 infection directly and indirectly causes dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction, which interact with each other and are exacerbated by cardiovascular risk factors. In this review, we summarize current knowledge on the pathogenic basis of thromboinflammation and endothelial injury in COVID-19. We highlight the distinct contributions of dysregulated immune responses, platelet hyperactivation, and endothelial dysfunction to the pathogenesis of COVID-19. In addition, we discuss potential therapeutic strategies targeting these mechanisms.

Indexed as

Angiotensin-Converting Enzyme 2Antiviral AgentsBlood CoagulationCOVID-19COVID-19 Drug TreatmentEndothelium, VascularHumansImmunity, InnatePlatelet ActivationSARS-CoV-2ThrombosisACE2 protein, humanAngiotensin-Converting Enzyme 2Antiviral AgentsCOVID-19endothelial injuryinflammationplatelet activationSARS-CoV-2therapeuticsthrombosis

Identifiers

PMID34769508
PMCPMC8584434
OpenAlexW3212393645

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.