Evidence map›Paper›PMID 17503113›Full record

ReviewClinical research in cardiology : official journal of the German Cardiac Society2007

Autoimmunological features in inflammatory cardiomyopathy.

Angela Kallwellis-Opara, Andrea Dörner, Wolfgang-Christian Poller, Michel Noutsias, Uwe Kühl, Heinz-Peter Schultheiss, Mathias Pauschinger

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical research in cardiology : official journal of the German Cardiac Society, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
3.4field-weighted citation impact, top 7% 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

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 58 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Immunogenic cell stress and death.Nature immunology · 2022
    Review
  11. Article
  12. Article
  13. Decompensated Heart Failure in Pregnancy.Cardiac failure review · 2016
    Article
  14. Article
  15. Elevated M2-muscarinic and β1-adrenergic receptor autoantibody levels are associated with paroxysmal atrial fibrillation.Clinical research in cardiology : official journal of the German Cardiac Society · 2015
    Observational
  16. Article
  17. Article
  18. TLR3 deficiency induces chronic inflammatory cardiomyopathy in resistant mice following coxsackievirus B3 infection: role for IL-4.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  19. Review
  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

7 authors at 1 institution in 1 country.

Angela Kallwellis-OparaCharité - Universitätsmedizin Berlin, Campus Benjamin-Franklin, Medizinische Klinik II, Abteilung für Kardiologie und Pneumologie, Hindenburgdamm 30, 12200 Berlin, Germany.
Andrea Dörner
Wolfgang-Christian Poller
Michel Noutsias
Uwe Kühl
Heinz-Peter Schultheiss
Mathias Pauschinger
Charité - Universitätsmedizin Berlin · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During recent years, increasing evidence has been obtained that cellular as well as humoral autoimmunity is involved in the pathogenesis of dilated cardiomyopathy (DCM). The immune system is generally activated by viral infections with the objective of virus elimination from the myocardium. However, a relevant number of patients demonstrate viral persistence and/or chronic inflammation in the myocardium. This chronic myocardial inflammation, defined by chronic inflammation, is termed "inflammatory cardiomyopathy" according to the WHO classification of cardiomyopathies. Chronic inflammation is frequently followed by the development of autoimmunity. A breakdown in the control mechanisms protecting against autoimmune reactions by both presentation of normally not accessible self-antigens and bystander- activation, induced by the pathogen, leads to the formation of autoreactive antibodies and T cells. The auto-reactive antibodies interact directly with heart tissue resulting in altered signal transduction or complement activation, whereas the T cell-mediated mechanisms include direct attack by cytotoxic T cells or indirect effects of cytotoxic cytokines released by stimulated T cells or macrophages.

Indexed as

AutoantibodiesAutoimmunityCytokinesHumansImmunity, CellularMyocarditisAutoantibodiesCytokines

Identifiers

PMID17503113
OpenAlexW2031434121

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.