Evidence map›Paper›PMID 23345411›Full record

ArticleJournal of lipid research2013

Cardiomyocyte-specific perilipin 5 overexpression leads to myocardial steatosis and modest cardiac dysfunction.

Hong Wang, Urmila Sreenivasan, Da-Wei Gong, Kelly A O'Connell, Erinne R Dabkowski, Peter A Hecker, Nicoleta Ionica, Manige Konig, Anup Mahurkar, Yezhou Sun and 2 more

Open access · hybridAbstract read
In one paragraph

Article in Journal of lipid research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 88 papers.

0numbers the graph read from it
0cells of the map it votes in
88citing papers in PubMed
7.9field-weighted citation impact, top 2% 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

88 citing papers in PubMed, 135 citations in OpenAlex.

  1. Article
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  5. Heterogeneity, dynamics and organelle interactions of lipid droplets.Nature reviews. Molecular cell biology · 2026
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  16. Lipotoxicity as a therapeutic target in obesity and diabetic cardiomyopathy.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2024
    Review
  17. Article
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28 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 1 country.

Hong WangDepartment of Medicine, School of Medicine, University of Maryland, Baltimore, MD, USA.
Urmila Sreenivasan
Da-Wei Gong
Kelly A O'Connell
Erinne R Dabkowski
Peter A Hecker
Nicoleta Ionica
Manige Konig
Anup Mahurkar
Yezhou Sun
William C Stanley
Carole Sztalryd
University of Maryland, Baltimore · USGeriatric Research Education and Clinical Center · USVA Maryland Health Care System · US

Funding

Research BaseP30DK072488 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI MITCHELL, BRAXTON D, TAYLOR, SIMEON I. · 2005 to 2019
$17.3M
Interdisciplinary Training Program Muscle BiologyT32AR007592 · NIAMS · UNIVERSITY OF MARYLAND BALTIMORE · PI Aikaterini Kontrogianni-Konstantopoulos · 1996 to 2026
$11.7M
JHU-UMD Diabetes Research CenterP30DK079637 · NIDDK · JOHNS HOPKINS UNIVERSITY · PI AHIMA, REXFORD S. · 2013 to 2017
$9.7M
Role of PAT proteins in ectopic fat depositionR01DK075017 · NIDDK · UNIVERSITY OF MARYLAND BALTIMORE · PI SZTALRYD, CAROLE A · 2007 to 2011
$1.4M
Intramural NIH HHSNIAMS NIH HHS T32 AR007592NIDDK NIH HHS 1-RO1-DK-075017NIDDK NIH HHS DK-072488NIDDK NIH HHS P30 DK072488NIDDK NIH HHS P30 DK079637NIDDK NIH HHS R01 DK075017
6 · The paper itself

Abstract

Presence of ectopic lipid droplets (LDs) in cardiac muscle is associated to lipotoxicity and tissue dysfunction. However, presence of LDs in heart is also observed in physiological conditions, such as when cellular energy needs and energy production from mitochondria fatty acid β-oxidation are high (fasting). This suggests that development of tissue lipotoxicity and dysfunction is not simply due to the presence of LDs in cardiac muscle but due at least in part to alterations in LD function. To examine the function of cardiac LDs, we obtained transgenic mice with heart-specific perilipin 5 (Plin5) overexpression (MHC-Plin5), a member of the perilipin protein family. Hearts from MHC-Plin5 mice expressed at least 4-fold higher levels of plin5 and exhibited a 3.5-fold increase in triglyceride content versus nontransgenic littermates. Chronic cardiac excess of LDs was found to result in mild heart dysfunction with decreased expression of peroxisome proliferator-activated receptor (PPAR)α target genes, decreased mitochondria function, and left ventricular concentric hypertrophia. Lack of more severe heart function complications may have been prevented by a strong increased expression of oxidative-induced genes via NF-E2-related factor 2 antioxidative pathway. Perilipin 5 regulates the formation and stabilization of cardiac LDs, and it promotes cardiac steatosis without major heart function impairment.

Indexed as

AnimalsBlotting, WesternCardiomyopathiesCell LineCricetinaeDNA, MitochondrialMiceMice, TransgenicMicroscopy, Electron, TransmissionMolecular Sequence DataMyocardiumMyocytes, CardiacPerilipin-5ProteinsReactive Oxygen SpeciesTriglyceridesDNA, MitochondrialPerilipin-5Plin5 protein, mouseProteinsReactive Oxygen SpeciesTriglycerides

Identifiers

PMID23345411
PMCPMC3606001
OpenAlexW2032518511

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.