Evidence map›Paper›PMID 19228708›Full record

ArticleCardiovascular research2009

Sphingosine-1-phosphate and sphingosine kinase are critical for transforming growth factor-beta-stimulated collagen production by cardiac fibroblasts.

Nicole Gellings Lowe, James S Swaney, Kelli M Moreno, Roger A Sabbadini

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
2.5field-weighted citation impact, top 11% 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

75 citing papers in PubMed, 142 citations in OpenAlex.

  1. Sphingomyelin as a key negative mediator in atrial fibrillation via lipid profiling analysis and functional identification.Europace : European pacing, arrhythmias, and cardiac electrophysiology : journal of the working groups on cardiac pacing, arrhythmias, and cardiac cellular electrophysiology of the European Society of Cardiology · 2026
    Article
  2. Review
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  4. Article
  5. The E2F family: a ray of dawn in cardiomyopathy.Molecular and cellular biochemistry · 2025
    Review
  6. Review
  7. Article
  8. Sphingolipids: drivers of cardiac fibrosis and atrial fibrillation.Journal of molecular medicine (Berlin, Germany) · 2024
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Effects of RAGE Deletion on the Cardiac Transcriptome during Aging.International journal of molecular sciences · 2022
    Article
  15. Article
  16. Article
  17. Review
  18. Sphingolipid metabolism and signaling in cardiovascular diseases.Frontiers in cardiovascular medicine · 2022
    Review
  19. Article
  20. Sphingosine 1-Phosphate-Upregulated COX-2/PGEOxidative medicine and cellular longevity · 2022
    Article

15 more citing papers are in PubMed but not listed here.

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.

Nicole Gellings LoweDepartment of Biology, San Diego State University, 5500 Campanile Dr, San Diego, CA 92182-4614, USA.
James S Swaney
Kelli M Moreno
Roger A Sabbadini
San Diego State University · USLpath (United States) · US

Funding

Role of Sphingolipids in Cardiac IschemiaR43HL075906 · NHLBI · LPATH THERAPEUTICS, INC. · PI SABBADINI, ROGER ALLEN · 2004 to 2004
$153k
NHLBI NIH HHS HL075906-01NHLBI NIH HHS R43 HL075906
6 · The paper itself

Abstract

aimsFollowing injury, fibroblasts transform into myofibroblasts and produce extracellular matrix (ECM). Excess production of ECM associated with cardiac fibrosis severely inhibits cardiac function. Sphingosine-1-phosphate (S1P), a bioactive lysophospholipid, regulates the function of numerous cell types. In this study, we determined the role of S1P in promoting pro-fibrotic actions of cardiac fibroblasts (CFs). METHODS AND

resultsS1P-mediated effects on myofibroblast transformation, collagen production, and cross-talk with transforming growth factor-beta (TGF-beta) using mouse CF were examined. S1P increased alpha-smooth muscle actin (a myofibroblast marker) and collagen expression in a S1P2 receptor- and Rho kinase-dependent manner. TGF-beta increased sphingosine kinase 1 (SphK1; the enzyme responsible for S1P production) expression and activity. TGF-beta-stimulated collagen production was inhibited by SphK1 or S1P2 siRNA, a SphK inhibitor, and an anti-S1P monoclonal antibody.

conclusionThese findings suggest that TGF-beta-stimulated collagen production in CF involves 'inside-out' S1P signalling whereby S1P produced intracellularly by SphK1 can be released and act in an autocrine/paracrine fashion to activate S1P2 and increase collagen production.

Indexed as

AnimalsAntibodies, MonoclonalCell DifferentiationCells, CulturedCollagenEnzyme InhibitorsFibroblastsLymphotoxin-alphaLysophospholipidsMaleMiceMice, Inbred C57BLMyocardiumPhosphotransferases (Alcohol Group Acceptor)rho-Associated KinasesRNA, Small InterferingAntibodies, MonoclonalCollagenEnzyme InhibitorsLymphotoxin-alphaLysophospholipidsPhosphotransferases (Alcohol Group Acceptor)rho-Associated KinasesRNA, Small InterferingSphingosinesphingosine 1-phosphateSphingosine Kinase

Identifiers

PMID19228708
PMCPMC2675932
OpenAlexW2167630574

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.