Evidence map›Paper›PMID 25968336›Full record

ArticleJournal of molecular and cellular cardiology2015

Functional brown adipose tissue limits cardiomyocyte injury and adverse remodeling in catecholamine-induced cardiomyopathy.

Robrecht Thoonen, Laura Ernande, Juan Cheng, Yasuko Nagasaka, Vincent Yao, Alexandre Miranda-Bezerra, Chan Chen, Wei Chao, Marcello Panagia, David E Sosnovik and 6 more

Registry-linked trialOpen access · bronzeAbstract read
In one paragraph

Article in Journal of molecular and cellular cardiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03793127 (BAT as a Therapeutic for the Metabolic and Cardiac Dysfunction With Senescence Pilot), which is not on this map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
2.8field-weighted citation impact, top 10% 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.

NCT03793127 active not recruitingnot on this mapstarted 2019, after this paper: background citation

BAT as a Therapeutic for the Metabolic and Cardiac Dysfunction With Senescence Pilot

TypeobservationalSponsorAdventHealth Translational Research InstituteRan2019 to 2025Enrolled24ConditionsAgingArmsMaximal oxygen consumption (V02 max), Brown adipose tissue (BAT) imaging, Muscle function testing
3 · Its place in the literature

Who cites it

50 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
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  11. UCP1-dependent brown adipose activation accelerates cardiac metabolic remodeling and reduces initial hypertrophic and fibrotic responses to pathological stress.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 2 institutions in 3 countries.

Robrecht ThoonenCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA.
Laura ErnandeCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA; DHU Ageing Thorax Vessels Blood, Inserm Unit 955 Team 08, Faculté de Medecine de Créteil, Hôpital Henri Mondor, AP-HP, Créteil, France.
Juan ChengCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA; Department of Ultrasound, Xinhua Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Yasuko NagasakaCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA; Department of Anesthesia and Critical Pain, Massachusetts General Hospital, Boston, MA, USA.
Vincent YaoCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA.
Alexandre Miranda-BezerraCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA.
Chan ChenDepartment of Anesthesia and Critical Pain, Massachusetts General Hospital, Boston, MA, USA.
Wei ChaoDepartment of Anesthesia and Critical Pain, Massachusetts General Hospital, Boston, MA, USA.
Marcello PanagiaCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA.
David E SosnovikCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA.
Dheeraj PuppalaCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA.
Antonis A ArmoundasCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA.
Allyson HindleDepartment of Anesthesia and Critical Pain, Massachusetts General Hospital, Boston, MA, USA.
Kenneth D BlochCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA; Department of Anesthesia and Critical Pain, Massachusetts General Hospital, Boston, MA, USA.
Emmanuel S BuysDepartment of Anesthesia and Critical Pain, Massachusetts General Hospital, Boston, MA, USA.
Marielle Scherrer-CrosbieCardiovascular Research Center, Massachusetts General Hospital, Boston, MA, USA. Electronic address: marielle@crosbie.com.
Massachusetts General Hospital · USAssistance Publique – Hôpitaux de Paris · FR

Funding

Detection of Brown Adipose Tissue Using Contrast UltrasoundR21DK092909 · NIDDK · MASSACHUSETTS GENERAL HOSPITAL · PI SCHERRER-CROSBIE, MARIELLE · 2011 to 2012
$450k
NIDDK NIH HHS R21 DK092909NIDDK NIH HHS R21-DK092909
6 · The paper itself

Abstract

Brown adipose tissue (BAT) has well recognized thermogenic properties mediated by uncoupling protein 1 (UCP1); more recently, BAT has been demonstrated to modulate cardiovascular risk factors. To investigate whether BAT also affects myocardial injury and remodeling, UCP1-deficient (UCP1(-/-)) mice, which have dysfunctional BAT, were subjected to catecholamine-induced cardiomyopathy. At baseline, there were no differences in echocardiographic parameters, plasma cardiac troponin I (cTnI) or myocardial fibrosis between wild-type (WT) and UCP1(-/-) mice. Isoproterenol infusion increased cTnI and myocardial fibrosis and induced left ventricular (LV) hypertrophy in both WT and UCP1(-/-) mice. UCP1(-/-) mice also demonstrated exaggerated myocardial injury, fibrosis, and adverse remodeling, as well as decreased survival. Transplantation of WT BAT to UCP1(-/-) mice prevented the isoproterenol-induced cTnI increase and improved survival, whereas UCP1(-/-) BAT transplanted to either UCP1(-/-) or WT mice had no effect on cTnI release. After 3 days of isoproterenol treatment, phosphorylated AKT and ERK were lower in the LV's of UCP1(-/-) mice than in those of WT mice. Activation of BAT was also noted in a model of chronic ischemic cardiomyopathy, and was correlated to LV dysfunction. Deficiency in UCP1, and accompanying BAT dysfunction, increases cardiomyocyte injury and adverse LV remodeling, and decreases survival in a mouse model of catecholamine-induced cardiomyopathy. Myocardial injury and decreased survival are rescued by transplantation of functional BAT to UCP1(-/-) mice, suggesting a systemic cardioprotective role of functional BAT. BAT is also activated in chronic ischemic cardiomyopathy.

Indexed as

Ventricular RemodelingAdipose Tissue, BrownAnimalsBiomarkersBlood PressureBody WeightCardiomyopathiesCardiotonic AgentsCatecholaminesExtracellular Signal-Regulated MAP KinasesFibrosisGene Expression RegulationHeart FailureHeart VentriclesIon ChannelsIsoproterenolBiomarkersCardiotonic AgentsCatecholaminesExtracellular Signal-Regulated MAP KinasesIon ChannelsIsoproterenolMitochondrial ProteinsProto-Oncogene Proteins c-aktUcp1 protein, mouseUncoupling Protein 1Brown adipose tissueCardioprotectionHeart failureIsoproterenolUncoupling protein 1

Identifiers

PMID25968336
PMCPMC4470477
OpenAlexW1897668887

What OpenQuestion holds

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Read underepoch 390

Registered trials

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.