Evidence map›Paper›PMID 33032170›Full record

ArticleMedical hypotheses2020

SARS-CoV-2 cell entry receptor ACE2 mediated endothelial dysfunction leads to vascular thrombosis in COVID-19 patients.

Ashutosh Kumar, Ravi K Narayan, Chiman Kumari, Muneeb A Faiq, Maheswari Kulandhasamy, Kamla Kant, Vikas Pareek

Open access · greenAbstract read
In one paragraph

Article in Medical hypotheses, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 9% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 5 institutions in 2 countries.

Ashutosh KumarEtiologically Elusive Disorders Research Network (EEDRN), New Delhi, India; Department of Anatomy, All India Institute of Medical Sciences (AIIMS), Patna, India. Electronic address: drashutoshkumar@aiimspatna.org.
Ravi K NarayanEtiologically Elusive Disorders Research Network (EEDRN), New Delhi, India; Department of Anatomy, All India Institute of Medical Sciences (AIIMS), Patna, India.
Chiman KumariEtiologically Elusive Disorders Research Network (EEDRN), New Delhi, India; Department of Anatomy, Postgraduate Institute of Medical Education and Research (PGIMER), Chandigarh, India.
Muneeb A FaiqEtiologically Elusive Disorders Research Network (EEDRN), New Delhi, India; New York University (NYU) Langone Health Center, NYU Robert I Grossman School of Medicine, New York, NY, USA.
Maheswari KulandhasamyEtiologically Elusive Disorders Research Network (EEDRN), New Delhi, India; Department of Biochemistry, Maulana Azad Medical College (MAMC), New Delhi, India.
Kamla KantEtiologically Elusive Disorders Research Network (EEDRN), New Delhi, India; Department of Microbiology, All India Institute of Medical Sciences (AIIMS), Bathinda, India.
Vikas PareekEtiologically Elusive Disorders Research Network (EEDRN), New Delhi, India; National Brain Research Center, Manesar, Haryana, India.
Education and Research Network · INAll India Institute of Medical Sciences · INMaulana Azad Medical College · INNational Brain Research Centre · INNew York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Several studies have described unusually high incidence of vascular thrombosis in coronavirus disease-2019 (COVID-19) patients. Pathogenesis of the vascular thrombosis in COVID-19 is least understood for now and presents a challenge to the treating physicians. Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), the causative pathogen for COVID-19, has been shown to bind to angiotensin converting enzyme 2 (ACE2) protein in human epithelial cells which facilitates its entry in the organ and mediate tissue specific pathogenesis. For ACE2 mediated cell entry of the SARS-CoV-2, co-expression of one more protein-Transmembrane protease serine 2 (TMPRSS2) is essential. Existing studies suggested significant expression of ACE2 and TMPRSS2 in human vascular endothelium. Vascular endothelial dysfunction can potentially activate coagulation cascade eventually resulting in thrombosis. ACE2 has proven role in the maintenance of endothelial integrity inside the vessels. Existing in situ evidence for SARS-CoV-1 (the causative agent for SARS pandemic of 2002, which shared ACE2 as cell entry receptor) suggested that virus binding can downregulate ACE2, thus can induce endothelial dysfunction. Recently, in situ evidence has been presented that SARS-CoV-2 can infect cells in engineered human vascular endothelium, which can be effectively blocked by using clinical-grade recombinant human ACE2. Based on the circumstantial evidence present in the literature, we propose a SARS-CoV-2 cell entry receptor ACE2 based mechanism for vascular thrombosis in COVID-19 patients.

Indexed as

Angiotensin-Converting Enzyme 2COVID-19Endothelium, VascularHumansRecombinant ProteinsSARS-CoV-2Serine EndopeptidasesSignal TransductionThrombosisTreatment OutcomeVascular DiseasesVirus InternalizationACE2 protein, humanAngiotensin-Converting Enzyme 2Recombinant ProteinsSerine EndopeptidasesTMPRSS2 protein, humanACE2COVID-19SARS-CoV-2ThrombosisTMPRSS2Vascular endothelial dysfunction

Identifiers

PMID33032170
PMCPMC7525265
OpenAlexW3089412566

What OpenQuestion holds

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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.