Evidence map›Paper›PMID 11909974›Full record

ArticleMolecular and cellular biology2002

Impaired cardiac contractility response to hemodynamic stress in S100A1-deficient mice.

Xiao-Jun Du, Timothy J Cole, Nora Tenis, Xiao-Ming Gao, Frank Köntgen, Bruce E Kemp, Jörg Heierhorst

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.7field-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

47 citing papers in PubMed, 123 citations in OpenAlex.

  1. Review
  2. Structural insights into the regulation of RyR1 by S100A1.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Changes of calcium cycling in HFrEF and HFpEF.Mechanobiology in medicine · 2023
    Review
  4. Article
  5. Review
  6. Targeting CaFrontiers in physiology · 2020
    Review
  7. Current Landscape of Heart Failure Gene Therapy.Journal of the American Heart Association · 2019
    Review
  8. Loss of S100A1 expression leads to CaPhysiological reports · 2018
    Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Novel strategies for the treatment of heart failure.Rambam Maimonides medical journal · 2012
    Article
  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

7 authors at 5 institutions in 2 countries.

Xiao-Jun DuBaker Medical Research Institute, Melbourne, Victoria 8008, Australia.
Timothy J Cole
Nora Tenis
Xiao-Ming Gao
Frank Köntgen
Bruce E Kemp
Jörg Heierhorst
Medical Research Institute · LKSt Vincents Institute of Medical Research · AUBaker Heart and Diabetes Institute · AUUniversity of Melbourne · AUWalter and Eliza Hall Institute of Medical Research · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ca(2+) signaling plays a central role in cardiac contractility and adaptation to increased hemodynamic demand. We have generated mice with a targeted deletion of the S100A1 gene coding for the major cardiac isoform of the large multigenic S100 family of EF hand Ca(2+)-binding proteins. S100A1(-/-) mice have normal cardiac function under baseline conditions but have significantly reduced contraction rate and relaxation rate responses to beta-adrenergic stimulation that are associated with a reduced Ca(2+) sensitivity. In S100A1(-/-) mice, basal left-ventricular contractility deteriorated following 3-week pressure overload by thoracic aorta constriction despite a normal adaptive hypertrophy. Surprisingly, heterozygotes also had an impaired response to acute beta-adrenergic stimulation but maintained normal contractility in response to chronic pressure overload that coincided with S100A1 upregulation to wild-type levels. In contrast to other genetic models with impaired cardiac contractility, loss of S100A1 did not lead to cardiac hypertrophy or dilation in aged mice. The data demonstrate that high S100A1 protein levels are essential for the cardiac reserve and adaptation to acute and chronic hemodynamic stress in vivo.

Indexed as

Adrenergic beta-AgonistsAgingAnimalsCalcium-Binding ProteinsCalcium SignalingGene TargetingHeart VentriclesHemodynamicsHeterozygoteIsoproterenolMiceMice, Inbred C57BLMice, KnockoutMyocardial ContractionReceptors, Adrenergic, betaS100 ProteinsAdrenergic beta-AgonistsCalcium-Binding ProteinsIsoproterenolReceptors, Adrenergic, betaS100A1 proteinS100 Proteins

Identifiers

PMID11909974
PMCPMC133731
OpenAlexW2147368435

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.