Evidence map›Paper›PMID 24013804›Full record

ArticleCardiovascular drugs and therapy2013

Docosahexaenoic acid supplementation alters key properties of cardiac mitochondria and modestly attenuates development of left ventricular dysfunction in pressure overload-induced heart failure.

Erinne R Dabkowski, Kelly A O'Connell, Wenhong Xu, Eduardo Hertel Ribeiro, Peter A Hecker, Kadambari Chandra Shekar, Caroline Daneault, Christine Des Rosiers, William C Stanley

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular drugs and therapy, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

16 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Omega-3 fatty acids in the treatment of heart failure.Current problems in cardiology · 2024
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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

9 authors at 4 institutions in 3 countries.

Erinne R DabkowskiDivision of Cardiology, Department of Medicine, University of Maryland, Baltimore, MD, USA.
Kelly A O'Connell
Wenhong Xu
Eduardo Hertel Ribeiro
Peter A Hecker
Kadambari Chandra Shekar
Caroline Daneault
Christine Des Rosiers
William C Stanley
University of Maryland, College Park · USUniversité de Montréal · CAUniversity of Maryland, Baltimore · USUniversity of Sydney · AU

Funding

Substrate Selection and Oxidative Stress in Heart FailureP01HL074237 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STANLEY, WILLIAM C · 2003 to 2013
$19.9M
Interdisciplinary Training Program Muscle BiologyT32AR007592 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI Aikaterini Kontrogianni-Konstantopoulos · 1996 to 2026
$11.7M
Docosahexaenoic Acid for Treatment of Heart FailureP20HL101434 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI MEHRA, MANDEEP R, STANLEY, WILLIAM C · 2010 to 2011
$1.3M
Docosahexaenoic Acid, Mitochondrial Dysfunction and Cardiac Reperfusion InjuryR21HL110731 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STANLEY, WILLIAM C · 2011 to 2012
$422k
NHLBI NIH HHS P01 HL074237NHLBI NIH HHS P20 HL101434NHLBI NIH HHS R21 HL110731NIAMS NIH HHS T32 AR007592
6 · The paper itself

Abstract

purposeSupplementation with the n3 polyunsaturated fatty acid docosahexaenoic acid (DHA) is beneficial in heart failure patients, however the mechanisms are unclear. DHA is incorporated into membrane phospholipids, which may prevent mitochondrial dysfunction. Thus we assessed the effects of DHA supplementation on cardiac mitochondria and the development of heart failure caused by aortic pressure overload.

methodsPathological cardiac hypertrophy was generated in rats by thoracic aortic constriction. Animals were fed either a standard diet or were supplemented with DHA (2.3 % of energy intake).

resultsAfter 14 weeks, heart failure was evident by left ventricular hypertrophy and chamber enlargement compared to shams. Left ventricle fractional shortening was unaffected by DHA treatment in sham animals (44.1 ± 1.6 % vs. 43.5 ± 2.2 % for standard diet and DHA, respectively), and decreased with heart failure in both treatment groups, but to a lesser extent in DHA treated animals (34.9 ± 1.7 %) than with the standard diet (29.7 ± 1.5 %, P < 0.03). DHA supplementation increased DHA content in mitochondrial phospholipids and decreased membrane viscosity. Myocardial mitochondrial oxidative capacity was decreased by heart failure and unaffected by DHA. DHA treatment enhanced Ca(2+) uptake by subsarcolemmal mitochondria in both sham and heart failure groups. Further, DHA lessened Ca(2+)-induced mitochondria swelling, an index of permeability transition, in heart failure animals. Heart failure increased hydrogen peroxide-induced mitochondrial permeability transition compared to sham, which was partially attenuated in interfibrillar mitochondria by treatment with DHA.

conclusionsDHA decreased mitochondrial membrane viscosity and accelerated Ca(2+) uptake, and attenuated susceptibility to mitochondrial permeability transition and development of left ventricular dysfunction.

Indexed as

Dietary SupplementsAnimalsArachidonic AcidDocosahexaenoic AcidsHeart FailureMaleMitochondria, HeartPhospholipidsPressureRatsRats, Sprague-DawleyVentricular Dysfunction, LeftArachidonic AcidDocosahexaenoic AcidsPhospholipids

Identifiers

PMID24013804
PMCPMC4364545
OpenAlexW2037197248

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.