Evidence map›Paper›PMID 22930739›Full record

ArticlePhysiological genomics2012

Quantitative proteomic analysis reveals novel mitochondrial targets of estrogen deficiency in the aged female rat heart.

T S Lancaster, S J Jefferson, J Craig Hunter, Veronica Lopez, J E Van Eyk, E G Lakatta, D H Korzick

Abstract read
In one paragraph

Article in Physiological genomics, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.9field-weighted citation impact, top 9% 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

24 citing papers in PubMed, 34 citations in OpenAlex.

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  13. Mitochondria and ageing: role in heart, skeletal muscle and adipose tissue.Journal of cachexia, sarcopenia and muscle · 2017
    Review
  14. Article
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  17. Article
  18. Review
  19. Estrogen and the female heart.Molecular and cellular endocrinology · 2014
    Review
  20. 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

7 authors at 3 institutions in 1 country.

T S LancasterDepartment of Kinesiology, The Pennsylvania State University, University Park, Pennsylvania 16802, USA.
S J Jefferson
J Craig Hunter
Veronica Lopez
J E Van Eyk
E G Lakatta
D H Korzick
Pennsylvania State University · USInstitute on Aging · USJohns Hopkins Medicine · US

Funding

Mitochondrial and Nuclear Mechanisms of Estrogen Receptor-Mediated CardioprotectiR01HL091097 · NHLBI · PENNSYLVANIA STATE UNIVERSITY, THE · PI KORZICK, DONNA HOPE · 2009 to 2012
$1.7M
Novel Mitochondrial Mechanisms of Ethanol-Induced Cardiac Injury in Aged FemalesRC2AA019403 · NIAAA · PENNSYLVANIA STATE UNIVERSITY, THE · PI KORZICK, DONNA HOPE · 2009 to 2010
$1.0M
Intramural NIH HHSNHLBI NIH HHS HL-091097NHLBI NIH HHS HL-091097-01A2S1NIAAA NIH HHS AA-019403
6 · The paper itself

Abstract

The incidence of myocardial infarction rises sharply at menopause, implicating a potential role for estrogen (E(2)) loss in age-related increases in ischemic injury. We aimed to identify quantitative changes to the cardiac mitochondrial proteome of aging females, based on the hypothesis that E(2) deficiency exacerbates age-dependent disruptions in mitochondrial proteins. Mitochondria isolated from left ventricles of adult (6 mo) and aged (24 mo) F344 ovary-intact or ovariectomized (OVX) rats were labeled with 8plex isobaric tags for relative and absolute quantification (iTRAQ; n = 5-6/group). Groups studied were adult, adult OVX, aged, and aged OVX. In vivo coronary artery ligation and in vitro mitochondrial respiration studies were also performed in a subset of rats. We identified 965 proteins across groups and significant directional changes in 67 proteins of aged and/or aged OVX; 32 proteins were unique to aged OVX. Notably, only six proteins were similarly altered in adult OVX (voltage-dependent ion channel 1, adenine nucleotide translocator 1, cytochrome c oxidase subunits VIIc and VIc, catalase, and myosin binding protein C). Proteins affected by aging were primarily related to cellular metabolism, oxidative stress, and cell death. The largest change occurred in monoamine oxidase-A (MAO-A), a source of oxidative stress. While acute MAO-A inhibition induced mild uncoupling in aged mitochondria, reductions in infarct size were not observed. Age-dependent alterations in mitochondrial signaling indicate a highly selective myocardial response to E(2) deficiency. The combined proteomic and functional approaches described here offer possibility of new protein targets for experimentation and therapeutic intervention in the aged female population.

Indexed as

AnimalsEstrogensFemaleHeartHeart VentriclesMitochondriaMonoamine OxidaseMyocardial IschemiaMyocardiumOvaryOxygen ConsumptionProteomicsRatsRats, Inbred F344EstrogensMonoamine Oxidase

Identifiers

PMID22930739
PMCPMC3472466
OpenAlexW2160305464

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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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.