Evidence map›Paper›PMID 20559771›Full record

ArticleJournal of cardiovascular translational research2010

Dichotomous actions of NF-kappaB signaling pathways in heart.

Rimpy Dhingra, James A Shaw, Yaron Aviv, Lorrie A Kirshenbaum

Abstract read
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In one paragraph

Article in Journal of cardiovascular translational research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed, 1 pooled it
0.8field-weighted citation impact, top 24% 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

19 citing papers in PubMed, 1 synthesis or guideline pooled it, 36 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Article
  4. The Role of BAG3 Protein Interactions in Cardiomyopathies.International journal of molecular sciences · 2024
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  17. Redox signaling in cardiovascular health and disease.Free radical biology & medicine · 2013
    Review
  18. Review
  19. Cardiomyocyte-specific IκB kinase (IKK)/NF-κB activation induces reversible inflammatory cardiomyopathy and heart failure.Proceedings of the National Academy of Sciences of the United States of America · 2012
    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

4 authors at 2 institutions in 1 country.

Rimpy DhingraThe Institute of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Department of Physiology, Faculty of Medicine, University of Manitoba, Rm. 3016, 351 TachéAvenue, Winnipeg, MB, R2H 2A6, Canada.
James A Shaw
Yaron Aviv
Lorrie A Kirshenbaum
St. Boniface Hospital · CAUniversity of Manitoba · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

Despite the substantial progress in heart research over the past two decades heart failure still remains a major cause of morbidity and mortality in North America and is reaching pandemic proportions worldwide. Though the underlying causes are varied, the functional loss of contractile myocytes through apoptosis, necrosis, and autophagy has emerged a central unifying theme to explain diminished cardiac performance in individuals with heart failure. At the molecular level, there has been considerable interest in understanding the signaling pathways that regulate cell death in the heart with specific interest in the extrinsic and intrinsic cell death pathways. The cellular factor nuclear factor-kappaB (NF-kappaB) is a key transcription factor involved in the regulation of a wide range of genes involved in cellular process including inflammation, immune cell maturation, cell proliferation, and, most recently, cell survival. NF-kappaB signaling is important for the normal cellular growth and is a major target of inflammatory cytokines. Several studies have highlighted a protective role of NF-kappaB in the heart under certain circumstances including hypoxic or ischemic myocardial injury. The diverse nature and involvement of NF-kappaB in regulation of vital cellular processes including cell survival notably in the post-mitotic heart has sparked considerable interest in understanding the signaling pathways involved in regulating NF-kappaB in the heart under normal and pathological conditions. However, whether NF-kappaB is adaptive, maladaptive or is a homeostatic response to cardiac injury may simply depend on the context and timing of its activation. In this forum we discuss NF-kappaB signaling pathways and therapeutic opportunities to modulate NF-kappaB activity in heart failure.

Indexed as

HeartSignal TransductionApoptosisAutophagyBiomarkersCardiovascular DiseasesCell ProliferationCell SurvivalCytokinesHeart FailureHumansInflammationMyocardial Reperfusion InjuryMyocytes, CardiacNecrosisNF-kappa BBiomarkersCytokinesNF-kappa B

Identifiers

PMID20559771
OpenAlexW2059655076

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.