Evidence map›Paper›PMID 32676883›Full record

ReviewJournal of thrombosis and thrombolysis2021

COVID-19: the role of excessive cytokine release and potential ACE2 down-regulation in promoting hypercoagulable state associated with severe illness.

Fenghe Du, Bao Liu, Shuyang Zhang

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of thrombosis and thrombolysis, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 58 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
58citing papers in PubMed, 1 pooled it
2.1field-weighted citation impact, top 7% 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

58 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Narrative Review Explaining the Role ofInfectious disease reports · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. The controversial effect of smoking and nicotine in SARS-CoV-2 infection.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2023
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Interleukin 6: A biomarker for COVID-19 progression.Materials today. Proceedings · 2023
    Article
  19. Article
  20. The suboptimal fibrinolytic response in COVID-19 is dictated by high PAI-1.Journal of thrombosis and haemostasis : JTH · 2022
    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

3 authors at 1 institution in 1 country.

Fenghe DuDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan 1st, Dongcheng District, Beijing, 100730, China.
Bao LiuDepartment of Vascular Surgery, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan 1st, Dongcheng District, Beijing, 100730, China. liubao72@aliyun.com.ORCID http://orcid.org/0000-0001-6359-959X
Shuyang ZhangDepartment of Cardiology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Shuaifuyuan 1st, Dongcheng District, Beijing, 100730, China. shuyangzhang103@nrdrs.org.
Chinese Academy of Medical Sciences & Peking Union Medical College · CN

Funding

Beijing Municipal Science and Technology Commission "clinical application of capital characteristics" Z161100000516093Beijing Natural Science Foundation 7182131Chinese Academy of Medical Sciences Innovation Fund for Medical Sciences 2018-I2M-AI-004Non-profit Central Research Institute Fund of Chinese Academy of Medical Sciences 2019XK320004Peking Union Medical College Hospital Science Fund of Key Projects for Junior Faculty PUMCH-2016-1.20
6 · The paper itself

Abstract

The novel coronavirus disease (COVID-19) has become a universally prevalent infectious disease. The causative virus of COVID-19 is severe acute respiratory syndrome coronavirus type 2. Recent retrospective clinical studies have established a significant association between the incidence of vascular thrombotic events and the severity of COVID-19. The enhancement in serum levels of markers that reflect a hypercoagulable state has been suggested to indicate a poor prognosis. Therefore, at present, it is crucial to understand the mechanisms that foster the hypercoagulable state in COVID-19. Over-activated inflammatory response, which is manifested as excessive cytokine release in COVID-19 patients, is also associated with COVID-19 severity. This review discusses the immuno-pathological basis of the excessive cytokine release in COVID-19. Besides, this article reviews the role of pro-inflammatory or anti-inflammatory cytokines, whose significant elevations in their serum levels have been consistently detected in multiple different clinical studies, in promoting the hypercoagulable state. Since the expression of angiotensin-converting enzyme 2 (ACE2) is potentially down-regulated in COVID-19, as proposed by a recent bio-informatic analysis, mechanisms through which reduced ACE2 expressions promote vascular thrombosis are summarized. In addition, the reciprocal-enhancing effects of the excessive cytokine release and the downregulated ACE2 expression on their pro-thrombotic activities are further discussed. Here, based on currently available evidence, we review the pathogenic mechanisms of the hypercoagulable state associated with severe cases of COVID-19 to give insights into prevention and treatment of the vascular thrombotic events in COVID-19.

Indexed as

Down-RegulationAngiotensin-Converting Enzyme 2BiomarkersCOVID-19CytokinesHumansSARS-CoV-2Severity of Illness IndexThrombophiliaACE2 protein, humanAngiotensin-Converting Enzyme 2BiomarkersCytokinesACE2COVID-19Excessive cytokine releaseHypercoagulable stateVascular thrombotic events

Identifiers

PMID32676883
PMCPMC7365308
OpenAlexW3043044167

What OpenQuestion holds

Textmetadata
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.