Evidence map›Paper›PMID 24904749›Full record

ReviewF1000prime reports2014

Learning from myocarditis: mimicry, chaos and black holes.

Noel R Rose

Open access · bronzeAbstract readReview
In one paragraph

Review in F1000prime reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.2field-weighted citation impact, top 12% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Review
  2. Infectious factors in myocarditis: a comprehensive review of common and rare pathogens.The Egyptian heart journal : (EHJ) : official bulletin of the Egyptian Society of Cardiology · 2024
    Review
  3. Review
  4. Review
  5. Article
  6. Implication of microRNA as a potential biomarker of myocarditis.Clinical and experimental pediatrics · 2022
    Article
  7. Fulminant myocarditis in adults: a narrative review.Journal of geriatric cardiology : JGC · 2022
    Article
  8. Article
  9. Update on acute myocarditis.Trends in cardiovascular medicine · 2021
    Review
  10. Article
  11. Circulating Exosomes Control CD4Molecular therapy : the journal of the American Society of Gene Therapy · 2020
    Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

1 author at 1 institution in 1 country.

Noel R RoseDepartments of Pathology and of Molecular Microbiology and Immunology, The Johns Hopkins Schools of Medicine and Public Health 615 North Wolfe Street, Baltimore, MD 21205 USA.
Johns Hopkins University · US

Funding

Pathogenesis of Autoimmune MyocarditisR01HL067290 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ROSE, NOEL R. · 2002 to 2009
$3.0M
Eosinophilic MyocarditisR01HL113008 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI CIHAKOVA, DANIELA · 2012 to 2015
$1.6M
Genetic mechanisms of autoimmune myocarditisR01HL077611 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ROSE, NOEL R. · 2004 to 2007
$1.4M
Genetic mechanisms of autoimmune myocarditisR56HL077611 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI ROSE, NOEL R. · 2009 to 2009
$369k
NHLBI NIH HHS R01 HL067290NHLBI NIH HHS R01 HL077611NHLBI NIH HHS R01 HL113008NHLBI NIH HHS R56 HL077611
6 · The paper itself

Abstract

Autoimmune myocarditis and its sequel, dilated cardiomyopathy, are major causes of heart failure, especially in children and young adults. We have developed animal models to investigate their pathogenesis by infecting genetically susceptible mice with coxsackievirus B3 or by immunizing them with cardiac myosin or its immunodominant peptide. A number of valuable lessons have emerged from our study of this paradigm of an infection-induced autoimmune disease. We understand more clearly how natural autoimmunity, as an important component of normal physiology, must be recalibrated regularly due to changes caused by infection or other internal and external stimuli. A new normal homeostatic platform will be established based on its evolutionary fitness. A loss of homeostasis with out-of-control normal autoimmunity leads to autoimmune disease. It is signified early on by a spread of an adaptive autoimmune response to novel epitopes and neighboring antigens. The progression from infection to normal, well-balanced autoimmunity to autoimmune disease and on to irreversible damage is a complex, step-wise process. Yet, chaos theory provides hope that the pattern is potentially predictable. Infection-induced autoimmune disease represents a sequence of events heading for a train wreck at the end of the line. Our aim in autoimmune disease research must be to stop the train before this happens.

Identifiers

PMID24904749
PMCPMC4018180
OpenAlexW2027575580

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.