Evidence map›Paper›PMID 23819990›Full record

ArticleCirculation research2013

Uncoupling protein 2 impacts endothelial phenotype via p53-mediated control of mitochondrial dynamics.

Yukio Shimasaki, Ning Pan, Louis M Messina, Chunying Li, Kai Chen, Lijun Liu, Marcus P Cooper, Joseph A Vita, John F Keaney

Open access · bronzeAbstract read
In one paragraph

Article in Circulation research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.8field-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

22 citing papers in PubMed, 38 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 1 institution in 1 country.

Yukio ShimasakiFrom the Division of Cardiovascular Medicine, Department of Medicine.
Ning Pan
Louis M Messina
Chunying Li
Kai Chen
Lijun Liu
Marcus P Cooper
Joseph A Vita
John F Keaney
University of Massachusetts Chan Medical School · US

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
Nox4 and Vascular HomeostasisR01HL098407 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KEANEY, JOHN FRANCIS · 2010 to 2017
$3.8M
Mitochondrial Modulation of Endothelia FunctionR01HL092122 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KEANEY, JOHN FRANCIS · 2009 to 2016
$3.3M
Mitochondrial Dynamics and UCP2 - Endothelial Dysfunction in Human ObesityR01HL115391 · NHLBI · BOSTON UNIVERSITY MEDICAL CAMPUS · PI HAMBURG, NAOMI MIRIAM · 2013 to 2017
$2.8M
Mechanisms and metabolic implications of LRP130 in NAFLDR01DK089185 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI COOPER, MARCUS P · 2010 to 2014
$1.8M
NHLBI NIH HHS HL092122NHLBI NIH HHS HL098407NHLBI NIH HHS R01 HL092122NHLBI NIH HHS R01 HL098407NHLBI NIH HHS R01 HL115391NIDDK NIH HHS DK089185NIDDK NIH HHS DK32520NIDDK NIH HHS P30 DK032520NIDDK NIH HHS R01 DK089185
6 · The paper itself

Abstract

rationaleMitochondria, although required for cellular ATP production, are also known to have other important functions that may include modulating cellular responses to environmental stimuli. However, the mechanisms whereby mitochondria impact cellular phenotype are not yet clear.

objectiveTo determine how mitochondria impact endothelial cell function. METHODS AND

resultsWe report here that stimuli for endothelial cell proliferation evoke strong upregulation of mitochondrial uncoupling protein 2 (UCP2). Analysis in silico indicated increased UCP2 expression is common in highly proliferative cell types, including cancer cells. Upregulation of UCP2 was critical for controlling mitochondrial membrane potential (Δψ) and superoxide production. In the absence of UCP2, endothelial growth stimulation provoked mitochondrial network fragmentation and premature senescence via a mechanism involving superoxide-mediated p53 activation. Mitochondrial network fragmentation was both necessary and sufficient for the impact of UCP2 on endothelial cell phenotype.

conclusionsThese data identify a novel mechanism whereby mitochondria preserve normal network integrity and impact cell phenotype via dynamic regulation of UCP2.

Indexed as

Mitochondrial DynamicsPhenotypeAnimalsAortaCattleCell ProliferationCellular SenescenceEndothelial CellsIon ChannelsLungMembrane Potential, MitochondrialMiceMitochondriaMitochondrial ProteinsSuperoxidesTumor Suppressor Protein p53Ion ChannelsMitochondrial ProteinsSuperoxidesTumor Suppressor Protein p53Ucp2 protein, mouseUncoupling Protein 2angiogenesisendothelial functionendotheliumischemiamitochondriamitochondrial uncoupling proteinssuperoxides

Identifiers

PMID23819990
PMCPMC3869454
OpenAlexW2097896414

What OpenQuestion holds

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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.