Evidence map›Paper›PMID 21711241›Full record

ReviewCardiovascular & hematological agents in medicinal chemistry2011

Up-regulation of the cardiac lipid metabolism at the onset of heart failure.

Said Abdalla, Xuebin Fu, Sherif S Elzahwy, Kristin Klaetschke, Thomas Streichert, Ursula Quitterer

Open access · bronzeAbstract readReview
In one paragraph

Review in Cardiovascular & hematological agents in medicinal chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.7field-weighted citation impact, top 28% 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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
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  5. Role of Stearoyl-CoA Desaturase 1 in Cardiovascular Physiology.International journal of molecular sciences · 2023
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  11. Novel role of the ER/SR CaAmerican journal of physiology. Heart and circulatory physiology · 2019
    Article
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  13. Review
  14. Fatty acid synthase inhibits theThe Journal of biological chemistry · 2017
    Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. 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

6 authors at 5 institutions in 3 countries.

Said AbdallaMolecular Pharmacology Unit, Swiss Federal Institute of Technology and University of Zurich, Switzerland.
Xuebin Fu
Sherif S Elzahwy
Kristin Klaetschke
Thomas Streichert
Ursula Quitterer
University of Zurich · CHAin Shams University Hospital · EGÉcole Polytechnique Fédérale de Lausanne · CHUniversität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic pressure overload and atherosclerosis are primary etiologic factors for cardiac hypertrophy and failure. However, mechanisms underlying the transition from hypertrophy to heart failure are incompletely understood. We analyzed the development of heart failure in mice with chronic pressure overload induced by aortic constriction and compared the results with aged apolipoprotein E-deficient mice suffering from advanced atherosclerosis. We combined cardiac function analysis by echocardiography and invasive hemodynamics with a comprehensive microarray gene expression study (GSE25765-8). The microarray data showed that the onset of heart failure induced by pressure overload or advanced atherosclerosis was accompanied by a strong up-regulation of key lipid metabolizing enzymes involved in fat synthesis, storage and oxidation. Cardiac lipid overload may be involved in the progression of heart failure by enhancing cardiomyocyte death. Up-regulation of the cardiac lipid metabolism was related to oxygen and ATP depletion of failing hearts because anti-ischemic treatment with ranolazine normalized the cardiac lipid metabolism and improved cardiac function. Vice versa, inhibition of cellular respiration and ATP generation by mild thiol-blocking with cystamine triggered the cardiac lipid metabolism and caused signs of heart failure. Cardiac tissue specimens of patients with heart failure also showed high protein levels of key fat metabolizing enzymes as well as lipid accumulation. Taken together, our data strongly indicate that up-regulation of the cardiac lipid metabolism and myocardial lipid overload are underlying the development of heart failure.

Indexed as

Lipid MetabolismUp-RegulationAdenosine TriphosphateAnimalsAortic DiseasesAtherosclerosisHeart FailureHumansMiceMyocardiumOxygen ConsumptionAdenosine Triphosphate

Identifiers

PMID21711241
PMCPMC3319925
OpenAlexW2159692800

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.