Evidence map›Paper›PMID 20694832›Full record

ArticleHeart failure reviews2011

Innate immunity and remodelling.

Guro Valen

Abstract read
In one paragraph

Article in Heart failure reviews, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Observational
  8. The role of nitric oxide in regulation of leukocyte migration into the heart tissue in vitro.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2015
    Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Relationship of TLR2, TLR4 and tissue remodeling in chronic rhinosinusitis.International journal of clinical and experimental pathology · 2015
    Article
  14. Article
  15. Cardiomyocyte-specific p65 NF-κB deletion protects the injured heart by preservation of calcium handling.American journal of physiology. Heart and circulatory physiology · 2013
    Article
  16. Article
  17. Article
  18. Article
  19. Article
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.

Guro ValenDepartment of Physiology, Institute of Basic Medical Sciences, University of Oslo, Postbox 1103 Blindern, 0317, Oslo, Norway. guro.valen@medisin.uio.no

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A wide variety of cardiac disease states can induce remodelling and lead to the functional consequence of heart failure. These complex disease states involve a plethora of parallel signal transduction events, which may be associated with tissue injury or tissue repair. Innate immunity is activated in hearts injured in different ways, evident as cytokine release from the heart, activation of toll-like receptors involved in recognizing danger, and activation of the transcription factor nuclear factor kappa B. Nuclear factor kappa B regulates gene programmes involved in inflammation as well as the resolution of inflammation. The impact of this is an enigma; while cytokines, toll-like receptors, and nuclear factor kappa B appear to elicit myocardial protection in studies of preconditioning, the literature strongly indicates a detrimental role for activation of innate immunity in studies of acute ischaemia-reperfusion injury. The impact of activation of cardiac innate immunity on the long-term outcome in in vivo models of hypertrophy and remodelling is less clear, with conflicting results as to whether it is beneficial or detrimental. More research using genetically engineered mice as tools, different models of evoking remodelling, and long-term follow-up is required for us to conclude whether activation of the innate immune system is good, bad, or unimportant in chronic injury models.

Indexed as

Immunity, InnateVentricular RemodelingCytokinesHeart FailureHumansMyocardiumNF-kappa BToll-Like ReceptorsCytokinesNF-kappa BToll-Like Receptors

Identifiers

PMID20694832
PMCPMC3003782

What OpenQuestion holds

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Registered trials

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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.