Evidence map›Paper›PMID 33119197›Full record

ReviewJournal of thrombosis and haemostasis : JTH2021

Is there a role for the ACE2 receptor in SARS-CoV-2 interactions with platelets?

Robert A Campbell, Eric Boilard, Matthew T Rondina

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of thrombosis and haemostasis : JTH, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
2.0field-weighted citation impact, top 8% 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

59 citing papers in PubMed, 90 citations in OpenAlex.

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  20. FcFrontiers in cardiovascular medicine · 2023
    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

3 authors at 2 institutions in 2 countries.

Robert A CampbellUniversity of Utah Molecular Medicine Program, Salt Lake City, UT, USA.
Eric BoilardCentre de Recherche du Centre Hospitalier,, Universitaire de Québec- Université Laval, Québec, QC, Canada.
Matthew T RondinaUniversity of Utah Molecular Medicine Program, Salt Lake City, UT, USA.
University of Utah · USCentre hospitalier universitaire de Québec · CA

Funding

New Therapies to Restore Vascular Integrity During SepsisR01HL130541 · NHLBI · UNIVERSITY OF UTAH · PI ODELBERG, SHANNON J, WEYRICH, ANDREW S · 2016 to 2020
$3.7M
Translational Control of Megakaryocyte and Platelet Function in SepsisR01HL142804 · NHLBI · UNIVERSITY OF UTAH · PI RONDINA, MATTHEW THOMAS · 2018 to 2021
$1.9M
Platelet Immune Responses in Aging and InfluenzaR01AG048022 · NIA · UNIVERSITY OF UTAH · PI RONDINA, MATTHEW THOMAS · 2014 to 2018
$1.8M
Interferon-Induced Transmembrane Protein 3 (IFITM3) Regulates Thrombosis During Inflammation in AgingK01AG059892 · NIA · UNIVERSITY OF UTAH · PI CAMPBELL, ROBERT A · 2019 to 2022
$400k
Novel Regulatory Mechanisms of Inflammation-Induced ThrombosisR56AG059877 · NIA · UNIVERSITY OF UTAH · PI RONDINA, MATTHEW THOMAS · 2018 to 2018
$381k
Platelet Reprogramming During InflammationI01CX001696 · VA · VA SALT LAKE CITY HEALTHCARE SYSTEM · PI Matthew Thomas Rondina · 2018 to 2026
–
CSRD VA I01 CX001696Fonds de Recherche du Québec en SantéNHLBI NIH HHS R01 HL130541NHLBI NIH HHS R01HL130541NHLBI NIH HHS R01 HL142804NHLBI NIH HHS R01HL142804NIA NIH HHS K01 AG059892NIA NIH HHS K01AG059892NIA NIH HHS R01 AG048022NIA NIH HHS R01AG048022NIA NIH HHS R56 AG059877NIA NIH HHS R56AG059877
6 · The paper itself

Abstract

There is an urgent need to understand the underlying mechanisms contributing to thrombotic and inflammatory complications during COVID-19. Data from independent groups have identified that platelets are hyperreactive during COVID-19. Platelet hyperreactivity is accompanied by changes in platelet gene expression, and enhanced interactions between platelets and leukocytes. In some patients, SARS-CoV-2 mRNA has been detected in platelets. Together, this suggests that SARS-CoV-2 may interact with platelets. However, controversy remains on which receptors mediate SARS-CoV-2 platelet interactions. Most, but not all, transcriptomic and proteomic analyses fail to observe the putative SARS-CoV-2 receptor, angiotensin converting enzyme-2, or the cellular serine protease necessary for viral entry, TMPRSS2, on platelets and megakaryocytes. Interestingly, platelets express other known SARS-CoV-2 receptors, which induce similar patterns of activation to those observed when platelets are incubated with SARS-CoV-2. This article explores these findings and discusses ongoing areas of controversy and uncertainty with regard to SARS-CoV-2 platelet interactions.

Indexed as

Angiotensin-Converting Enzyme 2Blood PlateletsCOVID-19Host Microbial InteractionsHumansMegakaryocytesModels, BiologicalPlatelet ActivationReceptors, VirusRNA, ViralSARS-CoV-2Serine EndopeptidasesThrombosisVirus InternalizationACE2 protein, humanAngiotensin-Converting Enzyme 2Receptors, VirusRNA, ViralSerine EndopeptidasesTMPRSS2 protein, humanACE2COVID-19plateletsSARS-CoV-2thrombosis

Identifiers

PMID33119197
PMCPMC7899240
OpenAlexW3095368690

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.