Evidence map›Paper›PMID 20819225›Full record

ArticleLipids in health and disease2010

ω-3 Polyunsaturated fatty acids prevent pressure overload-induced ventricular dilation and decrease in mitochondrial enzymes despite no change in adiponectin.

Karen M O'Shea, David J Chess, Ramzi J Khairallah, Peter A Hecker, Biao Lei, Kenneth Walsh, Christine Des Rosiers, William C Stanley

Open access · goldAbstract read
In one paragraph

Article in Lipids in health and disease, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

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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

8 authors at 3 institutions in 2 countries.

Karen M O'SheaDivision of Cardiology and Department of Medicine, University of Maryland, Baltimore, MD, USA.
David J Chess
Ramzi J Khairallah
Peter A Hecker
Biao Lei
Kenneth Walsh
Christine Des Rosiers
William C Stanley
University of Maryland, Baltimore · USBoston University · USMontreal Heart Institute · CA

Funding

Substrate Selection and Oxidative Stress in Heart FailureP01HL074237 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STANLEY, WILLIAM C · 2003 to 2013
$19.9M
REGULATION OF VESSEL WALL APOPTOSISR37AG015052 · NIA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI WALSH, KENNETH · 2003 to 2012
$4.0M
Docosahexaenoic Acid for Treatment of Heart FailureP20HL101434 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI MEHRA, MANDEEP R, STANLEY, WILLIAM C · 2010 to 2011
$1.3M
Omega-3 Fatty Acids and Heart FailureR21HL091307 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STANLEY, WILLIAM C · 2008 to 2009
$469k
NHLBI NIH HHS HL074237NHLBI NIH HHS HL091307NHLBI NIH HHS HL101434NIA NIH HHS R37 AG015052
6 · The paper itself

Abstract

backgroundPathological left ventricular (LV) hypertrophy frequently progresses to dilated heart failure with suppressed mitochondrial oxidative capacity. Dietary marine ω-3 polyunsaturated fatty acids (ω-3 PUFA) up-regulate adiponectin and prevent LV dilation in rats subjected to pressure overload. This study 1) assessed the effects of ω-3 PUFA on LV dilation and down-regulation of mitochondrial enzymes in response to pressure overload; and 2) evaluated the role of adiponectin in mediating the effects of ω-3 PUFA in heart.

methodsWild type (WT) and adiponectin-/- mice underwent transverse aortic constriction (TAC) and were fed standard chow ± ω-3 PUFA for 6 weeks. At 6 weeks, echocardiography was performed to assess LV function, mice were terminated, and mitochondrial enzyme activities were evaluated.

resultsTAC induced similar pathological LV hypertrophy compared to sham mice in both strains on both diets. In WT mice TAC increased LV systolic and diastolic volumes and reduced mitochondrial enzyme activities, which were attenuated by ω-3 PUFA without increasing adiponectin. In contrast, adiponectin-/- mice displayed no increase in LV end diastolic and systolic volumes or decrease in mitochondrial enzymes with TAC, and did not respond to ω-3 PUFA.

conclusionThese findings suggest ω-3 PUFA attenuates cardiac pathology in response to pressure overload independent of an elevation in adiponectin.

Indexed as

AdiponectinAnimalsBiomarkersFatty AcidsFatty Acids, Omega-3Fetal ProteinsFish OilsGene Expression RegulationHeart FailureHypertensionHypertrophy, Left VentricularMaleMiceMice, Inbred C57BLMice, KnockoutMitochondria, HeartAdiponectinBiomarkersFatty AcidsFatty Acids, Omega-3Fetal ProteinsFish OilsPhospholipidsRNA, Messenger

Identifiers

PMID20819225
PMCPMC2939588
OpenAlexW2043878863

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.