Evidence map›Paper›PMID 36982447›Full record

ReviewInternational journal of molecular sciences2023

COVID-19-Induced Myocarditis: Pathophysiological Roles of ACE2 and Toll-like Receptors.

Patrizia Pannucci, Sophie R Jefferson, Jonathan Hampshire, Samantha L Cooper, Stephen J Hill, Jeanette Woolard

Open access · goldFull text readReview
In one paragraph

Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
3.1field-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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Five-year cardiovascular outcomes following COVID-19-associated carditis.Clinical research in cardiology : official journal of the German Cardiac Society · 2026
    Article
  2. Review
  3. Review
  4. Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025
    Review
  5. Article
  6. Article
  7. Review
  8. Article
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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 2 institutions in 1 country.

Patrizia PannucciDivision of Physiology, Pharmacology and Neuroscience, School of Life Sciences, University of Nottingham, Nottingham NG7 2UH, UK.ORCID 0000-0002-1748-6911
Sophie R JeffersonSchool of Medicine, University of Nottingham, Nottingham NG7 2UH, UK.
Jonathan HampshireSchool of Medicine, University of Oxford, Oxford OX3 9DU, UK.ORCID 0000-0002-6135-7746
Samantha L CooperDivision of Physiology, Pharmacology and Neuroscience, School of Life Sciences, University of Nottingham, Nottingham NG7 2UH, UK.ORCID 0000-0002-9062-5893
Stephen J HillDivision of Physiology, Pharmacology and Neuroscience, School of Life Sciences, University of Nottingham, Nottingham NG7 2UH, UK.ORCID 0000-0002-4424-239X
Jeanette WoolardDivision of Physiology, Pharmacology and Neuroscience, School of Life Sciences, University of Nottingham, Nottingham NG7 2UH, UK.ORCID 0000-0001-5406-6847
University of Nottingham · GBUniversity of Oxford · GB

Funding

European Union GA 858070Medical Research Council MR/N020081/1
6 · The paper itself

Abstract

The clinical manifestations of the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection responsible for coronavirus disease 2019 (COVID-19) commonly include dyspnoea and fatigue, and they primarily involve the lungs. However, extra-pulmonary organ dysfunctions, particularly affecting the cardiovascular system, have also been observed following COVID-19 infection. In this context, several cardiac complications have been reported, including hypertension, thromboembolism, arrythmia and heart failure, with myocardial injury and myocarditis being the most frequent. These secondary myocardial inflammatory responses appear to be associated with a poorer disease course and increased mortality in patients with severe COVID-19. In addition, numerous episodes of myocarditis have been reported as a complication of COVID-19 mRNA vaccinations, especially in young adult males. Changes in the cell surface expression of angiotensin-converting enzyme 2 (ACE2) and direct injury to cardiomyocytes resulting from exaggerated immune responses to COVID-19 are just some of the mechanisms that may explain the pathogenesis of COVID-19-induced myocarditis. Here, we review the pathophysiological mechanisms underlying myocarditis associated with COVID-19 infection, with a particular focus on the involvement of ACE2 and Toll-like receptors (TLRs).

Indexed as

COVID-19MyocarditisAngiotensin-Converting Enzyme 2HumansPeptidyl-Dipeptidase ASARS-CoV-2Toll-Like ReceptorsAngiotensin-Converting Enzyme 2Peptidyl-Dipeptidase AToll-Like Receptorsangiotensin-converting enzyme 2 (ACE2)cardiovascular systemCOVID-19myocarditisSARS-CoV-2Toll-like receptors (TLRs)

Identifiers

PMID36982447
PMCPMC10049267
OpenAlexW4324060687

What OpenQuestion holds

Textfull text, public
LicenceCC BY
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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.