Evidence map›Paper›PMID 19234089›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2009

Sphingolipid signaling and treatment during remodeling of the uninfarcted ventricular wall after myocardial infarction.

Che-Chung Yeh, Hongzhe Li, Deepak Malhotra, Mei-Chuan Huang, Bo-Qing Zhu, Edward J Goetzl, Donald A Vessey, Joel S Karliner, Michael J Mann

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-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

17 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  7. βJournal of the American College of Cardiology · 2017
    Article
  8. Review
  9. Article
  10. Sphingolipid De Novo Biosynthesis: A Rheostat of Cardiovascular Homeostasis.Trends in endocrinology and metabolism: TEM · 2016
    Review
  11. Article
  12. Article
  13. Transcriptional profiling of HMGB1-induced myocardial repair identifies a key role for Notch signaling.Molecular therapy : the journal of the American Society of Gene Therapy · 2013
    Article
  14. Review
  15. Article
  16. Article
  17. 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

9 authors at 1 institution in 1 country.

Che-Chung YehCardiothoracic Surgery, 4150 Clement St., 112D, San Francisco, CA 94121, USA.
Hongzhe Li
Deepak Malhotra
Mei-Chuan Huang
Bo-Qing Zhu
Edward J Goetzl
Donald A Vessey
Joel S Karliner
Michael J Mann
St Clement's Hospital · GB

Funding

ERK Signaling and a Hybrid Surgical/Molecular Approach for Chronic Heart FailureR01HL083118 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MANN, MICHAEL J · 2006 to 2016
$4.2M
LYSOLIPID PHOSPHATE REGULATION OF LYMPHOCYTE FUNCTIONSR01HL031809 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI GOETZL, EDWARD J · 1985 to 2008
$2.5M
The role of S1P signaling in surgical cardiac remodelingK08HL079239 · NHLBI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MANN, MICHAEL J · 2006 to 2010
$609k
NHLBI NIH HHS 1K08-HL-079239NHLBI NIH HHS 1R01-HL-083118NHLBI NIH HHS 5R01-HL-31809
6 · The paper itself

Abstract

The sphingosine kinase (SphK)/sphingosine 1-phosphate (S1P) pathway, known to determine the fate and growth of various cell types, can enhance cardiac myocyte survival in vitro and provide cardioprotection in acute ex vivo heart preparations. However, the relevance of these findings to chronic cardiac pathology has never been demonstrated. We hypothesized that S1P signaling is impaired during chronic remodeling of the uninfarcted ventricle during the evolution of post-myocardial infarction (MI) cardiomyopathy and that a therapeutic enhancement of S1P signaling would ameliorate ventricular dysfunction. SphK expression and activity were measured in the remote, uninfarcted myocardium (RM) of C57Bl/6 mice subjected to coronary artery ligation. The mRNA expression of S1P receptor isoforms was also measured, as was the activation of the downstream S1P receptor mediators. A cardioprotective role for S1P(1) receptor agonism was tested via the administration of the S1P(1)-selective agonist SEW2871 during and after MI. As a result, the expression data suggested that a dramatic reduction in SphK activity in the RM early after MI may reflect a combination of posttranscriptional and posttranslational modulation. SphK activity continued to decline gradually during chronic post-MI remodeling, when S1P(1) receptor mRNA also fell below baseline. The S1P(1)-specific agonism with oral SEW2871 during the first 2-wk after MI reduced apoptosis in the RM and resulted in improved myocardial function, as reflected in the echocardiographic measurement of fractional shortening. In conclusion, these results provide the first documentation of alterations in S1P-mediated signaling during the in situ development of cardiomyopathy and suggest a possible therapeutic role for the pharmacological S1P receptor agonism in the post-MI heart.

Indexed as

AnimalsDisease Models, AnimalMaleMiceMice, Inbred C57BLMyocardial InfarctionMyocytes, CardiacOxadiazolesPhosphotransferases (Alcohol Group Acceptor)Receptors, LysosphingolipidRNA, MessengerSignal TransductionSphingolipidsSphingosine KinaseThiophenesVentricular RemodelingOxadiazolesPhosphotransferases (Alcohol Group Acceptor)Receptors, LysosphingolipidRNA, MessengerSEW2871SphingolipidsSphingosine KinaseThiophenes

Identifiers

PMID19234089
PMCPMC2670694
OpenAlexW2095856068

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.