Evidence map›Paper›PMID 26253472›Full record

ArticleBiochemical and biophysical research communications2015

Prevention of cardiac hypertrophy by the use of a glycosphingolipid synthesis inhibitor in ApoE-/- mice.

Sumita Mishra, Djahida Bedja, Christine Amuzie, Alberto Avolio, Subroto Chatterjee

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

14 citing papers in PubMed, 22 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Plasma sphingolipids and risk of cardiovascular diseases: a large-scale lipidomic analysis.Metabolomics : Official journal of the Metabolomic Society · 2020
    Article
  10. Review
  11. Article
  12. Review
  13. Getting to the heart of the sphingolipid riddle.Current opinion in physiology · 2018
    Article
  14. Review
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

5 authors at 1 institution in 1 country.

Sumita MishraJohns Hopkins University School of Medicine, Department of Pediatrics and Department of Medicine, Baltimore, USA.
Djahida BedjaJohns Hopkins University School of Medicine, Department of Cardiology, Baltimore, USA; Faculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Christine AmuzieJohns Hopkins University School of Medicine, Department of Pediatrics and Department of Medicine, Baltimore, USA.
Alberto AvolioFaculty of Medicine and Health Sciences, Macquarie University, Sydney, Australia.
Subroto ChatterjeeJohns Hopkins University School of Medicine, Department of Pediatrics and Department of Medicine, Baltimore, USA. Electronic address: schatte2@jhmi.edu.
Macquarie University · AU

Funding

Institute for Clinical and Translational ResearchUL1TR001079 · NCATS · JOHNS HOPKINS UNIVERSITY · PI FORD, DANIEL ERNEST · 2013 to 2017
$60.1M
Shared Resource CoresP01HL107153 · NHLBI · JOHNS HOPKINS UNIVERSITY · PI KASS, DAVID ALAN · 2011 to 2017
$16.8M
NCATS NIH HHS UL1 TR001079NHLBI NIH HHS P01 HL107153NHLBI NIH HHS P01HL10715301
6 · The paper itself

Abstract

ApoE-/- mice fed a high fat and high cholesterol (HFHC) diet (20% fat and 1.25% cholesterol) from 12 weeks of age to 36 weeks revealed an age-dependent increase in the left ventricular mass (LV mass) and decline in fractional shortening (FS%), which worsened with HFHC diet. These traits are indicative of maladaptive pathological cardiac hypertrophy and dysfunction. This was accompanied by loading of glycosphingolipids and increased gene expression of ANP, BNP in myocardial tissue. Masson's trichrome staining revealed a significant increase in cardiomyocyte size and fibrosis. In contrast, treatment with 5 and 10 μM D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of glucosylceramide synthase and lactosylceramide synthase, dose-dependently decreased the load of glycosphingolipids and preserved fractional shortening and maintained left ventricular mass to normal 12-week-old control levels over a 6 month treatment period. Our mechanistic studies showed that D-PDMP inhibited cardiac hypertrophy by inhibiting the phosphorylation of mitogen-activated protein kinase (MAPK). We propose that associating increased glycosphingolipid synthesis with cardiac hypertrophy could serve as a novel approach to prevent this phenotype in experimental animal models of diet -induced atherosclerotic heart disease.

Indexed as

AnimalsApolipoproteins EAtrial Natriuretic FactorCardiomegalyCardiotonic AgentsCholesterolDiet, High-FatEnzyme InhibitorsGalactosyltransferasesGene ExpressionGlucosyltransferasesGlycosphingolipidsHeart VentriclesMaleMiceMice, KnockoutApolipoproteins EAtrial Natriuretic FactorCardiotonic Agentsceramide glucosyltransferaseCholesterolEnzyme InhibitorsGalactosyltransferasesGlucosyltransferasesGlycosphingolipidsMitogen-Activated Protein KinasesMorpholinesNatriuretic Peptide, BrainRV 538UDPgalactose-glucosylceramide galactosyltransferaseAtherosclerotic heart diseaseCardiac hypertrophyGlycosphingolipidsLactosylceramide

Identifiers

PMID26253472
PMCPMC4888073
OpenAlexW1079401260

What OpenQuestion holds

Textmetadata
LicenceTDM
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.