Evidence map›Paper›PMID 11309527›Full record

ReviewHeart failure reviews2001

The role of interleukin-1 in the failing heart.

C S Long

Abstract readReview
PubMed Publisher
In one paragraph

Review in Heart failure reviews, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.9field-weighted citation impact, top 6% 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, 95 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Inflammation and the Heart: The Role of Traditional Factors.Cardiology research and practice · 2026
    Review
  4. Review
  5. Cardiac Fibroblasts and Myocardial Regeneration.Frontiers in bioengineering and biotechnology · 2021
    Review
  6. Frontiers in physiology · 2021
    Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Cardiac fibroblast in development and wound healing.Journal of molecular and cellular cardiology · 2014
    Review
  14. Review
  15. Review
  16. Review
  17. Review
  18. Origins of cardiac fibroblasts.Circulation research · 2010
    Review
  19. Cardiac fibroblast: the renaissance cell.Circulation research · 2009
    Review
  20. 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 at 1 institution in 1 country.

C S LongCardiology Section, Denver Health Medical Center, 777 Bannock St., Denver, CO 80204, USA. clong@dhha.org
Denver Health Medical Center · US

Funding

IL-1BETA REGULATES CARDIAC FIBROBLAST EXPRESSIONR01HL059428 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI LONG, CARLIN S · 1998 to 2005
$1.1M
IL1BETA INHIBITS CARDIOMYOCYTE SPECIFIC GENE EXPRESSIONR01HL058974 · NHLBI · UNIVERSITY OF COLORADO DENVER · PI LONG, CARLIN S · 1998 to 2001
$407k
NHLBI NIH HHS HL58974NHLBI NIH HHS HL59428
6 · The paper itself

Abstract

The prevalence of congestive heart failure and its continued poor prognosis despite presently available therapeutic options emphasize the importance of pursuing the observations suggesting an important role for an immunomodulatory approach to decompensated cardiac failure. Furthermore, there are several pieces of background information that suggest that cytokines like IL-1 may play a significant role in the pathogenesis of several forms of myocardial dysfunction. Although it seems clear that IL-1 is not acting alone under circumstances of myocardial injury, but in concert with other pro-inflammatory molecules and their effectors, we believe that continued investigations into the cytokine hypothesis will ultimately increase the understanding of how pro-inflammatory molecules influence myocardial function and how the modulation of such factors may improve the myocardial response to injury. The specific observations that emphasize the importance of pursuing a substantive role for IL-1 in this process are: (1) IL-1 is elevated in several cardiac disease states, (2) IL-1 is produced by myocardial cells themselves in response to injury, (3)The alterations in gene expression seen in response IL-1 resembles in many ways the phenotype of the failing heart, and (4) The co-localization of the IL-1 response with that of several previously described negative transcriptional regulators (making them potential targets for therapeutic manipulation).

Indexed as

AnimalsDisease ProgressionGene Expression RegulationHeart FailureHumansInterleukin-1MyosinsSignal TransductionTranscription FactorsInterleukin-1MyosinsTranscription Factors

Identifiers

PMID11309527
OpenAlexW1523775390

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.