Evidence map›Paper›PMID 28667560›Full record

ReviewAdvances in experimental medicine and biology2017

Cardiac Autoimmunity: Myocarditis.

William Bracamonte-Baran, Daniela Čiháková

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Advances in experimental medicine and biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 121 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
121citing papers in PubMed, 4 pooled it
60.9field-weighted citation impact, top 1% 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

121 citing papers in PubMed, 4 syntheses or guidelines pooled it, 227 citations in OpenAlex.

  1. Pooled it
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  7. Review
  8. TRIM21enhances IL-17A signaling and drives autoimmune myocarditis by promoting TRAF3 lysosomaldegradation in cardiac fibroblasts.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  19. Deep insight into cytokine storm: from pathogenesis to treatment.Signal transduction and targeted therapy · 2025
    Review
  20. Review

61 more citing papers are in PubMed but not listed here.

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

2 authors at 2 institutions in 1 country.

William Bracamonte-BaranDepartment of Pathology, Division of Immunology, Johns Hopkins University School of Medicine, 720 Rutland Ave., Baltimore, MD, 21205, USA.
Daniela ČihákováDivision of Immunology, Department of Pathology, Johns Hopkins University School of Medicine, 720 Rutland Ave., Baltimore, MD, 21205, USA. dcihako1@jhmi.edu.
Johns Hopkins Medicine · USJohns Hopkins University · US

Funding

Myeloid Cells are Critical in Inflammatory Heart DiseaseR01HL118183 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2014 to 2023
$4.4M
Eosinophilic MyocarditisR01HL113008 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2012 to 2015
$1.6M
NHLBI NIH HHS R01 HL113008NHLBI NIH HHS R01 HL118183
6 · The paper itself

Abstract

Myocarditis is the inflammation of the muscle tissues of the heart (myocardium). After a pathologic cardiac-specific inflammatory process, it may progress to chronic damage and dilated cardiomyopathy. The latter is characterized by systolic dysfunction, whose clinical correlate is heart failure. Nevertheless, other acute complications may arise as consequence of tissue damage and electrophysiologic disturbances. Different etiologies are involved in triggering myocarditis. In some cases, such as giant cell myocarditis or eosinophilic necrotizing myocarditis, it is an autoimmune process. Several factors predispose the development of autoimmune myocarditis such as systemic/local primary autoimmunity, viral infection, HLA and gender bias, exposure of cryptic antigens, mimicry, and deficient thymic training/Treg induction. Once the anti-myocardium autoimmune process is triggered, several components of the immune response orchestrate a sustained attack toward myocardial tissues with particular timing and immunopathogenic features. Innate response mediated by monocytes/macrophages, neutrophils, and eosinophils parallels the adaptive response, playing a final effector role and not only a priming function. Stromal cells like fibroblast are also involved in the process through specific cytokines. Furthermore, adaptive T cell responses have anti-paradigmatic features, as Th17 response is dispensable for acute myocarditis but is the main driver of the process leading to dilated cardiomyopathy. Humoral response, thought to be a bystander, is important in the appearance of late-stage hemodynamic complications. The complexity of that process, as well as the unspecific and variable clinical presentation, had generated difficulties for diagnosis and treatment, which remain suboptimal. In this chapter, we will discuss the most relevant immunopathogenic findings from a basic science and clinical perspective.

Indexed as

AutoimmunityAnimalsAutoimmune DiseasesDisease Models, AnimalHumansImmunosuppressive AgentsMyocarditisMyocardiumPrognosisRisk FactorsSignal TransductionImmunosuppressive AgentsAdaptive responseAutoimmunityDilated cardiomyopathyMyocarditis

Identifiers

PMID28667560
PMCPMC5706653
OpenAlexW2727000909

What OpenQuestion holds

Textmetadata
LicenceTDM
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.