Evidence map›Paper›PMID 20833647›Full record

ArticleCardiovascular research2011

Cardiac-specific leptin receptor deletion exacerbates ischaemic heart failure in mice.

Kenneth R McGaffin, William G Witham, Keith A Yester, Lia C Romano, Robert M O'Doherty, Charles F McTiernan, Christopher P O'Donnell

Open access · bronzeAbstract read
In one paragraph

Article in Cardiovascular research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 13% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 90 citations in OpenAlex.

  1. Pooled it
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  7. Role of Leptin in Obesity, Cardiovascular Disease, and Type 2 Diabetes.International journal of molecular sciences · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Kenneth R McGaffinCardiovascular Institute, University of Pittsburgh Medical Center, 1750 Bioscience Tower, 200 Lothrop Street, Pittsburgh, PA 15213, USA. mcgaffinkr@upmc.edu
William G Witham
Keith A Yester
Lia C Romano
Robert M O'Doherty
Charles F McTiernan
Christopher P O'Donnell
University of Pittsburgh Medical Center · US

Funding

Leptin Action and MacrophagesR01DK072162 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI O'DOHERTY, ROBERT M · 2006 to 2014
$2.7M
Sleep Apnea Links Obesity to Cardiovascular DysfunctionR01HL077785 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI O'DONNELL, CHRISTOPHER P · 2006 to 2010
$1.9M
Impact of Leptin of Heart Failure and Survival after Myocardial InfarctionK08HL087009 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI MCGAFFIN, KENNETH ROBERT · 2007 to 2011
$631k
NHLBI NIH HHS HL-077785NHLBI NIH HHS HL-087009NHLBI NIH HHS K08 HL087009NHLBI NIH HHS R01 HL077785NIDDK NIH HHS DK-072162NIDDK NIH HHS R01 DK072162
6 · The paper itself

Abstract

aimsthe obesity-related adipokine, leptin, has multiple actions on peripheral organs, including the mitigation of adverse cardiovascular outcomes after myocardial infarction (MI). Although we recently demonstrated that leptin, its receptor, and downstream signalling are up-regulated in the heart after MI, the significance of intact cardiomyoctye leptin signalling is unknown. Therefore, our objective was to generate a cardiomyocyte-specific leptin receptor knock-out (ObRKO) mouse to determine whether worse cardiac outcomes after MI result from impaired leptin signalling in cardiomyocytes. METHODS AND

resultstamoxifen-inducible ObRKO mice were subjected to experimental MI or sham surgeries and studied after 1 month. After MI, ObRKO mice displayed a loss of cardiac signal transducer and activator of transcription (STAT) 3 and adenosine monophosphate-activated protein kinase (AMPK) signalling. Worse survival and cardiac morbidity were also seen in the ObRKO mouse post-MI, including decreased contractile function and glycolytic metabolism, and increased left ventricular dilation, hypertrophy, collagen deposition, matrix metalloproteinase activity, apoptosis, and inflammation. Treatment of ObRKO mice post-MI with an ObR-independent AMPK activator improved cardiac function and restored many of these maladaptive processes to wild-type levels.

conclusionthese data indicate that leptin signalling mitigates cardiac injury in the post-MI failing heart by acting directly on cardiomyocytes to increase STAT3 and AMPK activation, to decrease cardiac hypertrophy, apoptosis, and inflammation, and to limit deleterious changes in cardiac structure, function, and glycolytic metabolism.

Indexed as

Aminoimidazole CarboxamideAMP-Activated Protein KinasesAnimalsEnzyme ActivationGlycolysisHeart FailureMaleMiceMice, Inbred C57BLMice, KnockoutModels, CardiovascularMyocardial InfarctionMyocardial IschemiaMyocytes, CardiacRibonucleotidesSignal TransductionAICA ribonucleotideAminoimidazole CarboxamideAMP-Activated Protein KinasesRibonucleotidesStat3 protein, mouseSTAT3 Transcription FactorTamoxifen

Identifiers

PMID20833647
PMCPMC3002875
OpenAlexW2129059128

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.