Evidence map›Paper›PMID 23381122›Full record

ArticleBasic research in cardiology2013

Cardiomyocyte-specific deletion of endothelin receptor A rescues aging-associated cardiac hypertrophy and contractile dysfunction: role of autophagy.

Asli F Ceylan-Isik, Maolong Dong, Yingmei Zhang, Feng Dong, Subat Turdi, Sreejayan Nair, Masashi Yanagisawa, Jun Ren

RetractedOpen access · greenAbstract readRetracted Publication
In one paragraph

Article in Basic research in cardiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
5.3field-weighted citation impact, top 4% 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

32 citing papers in PubMed, 67 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 2 countries.

Asli F Ceylan-IsikCenter for Cardiovascular Research and Alternative Medicine, University of Wyoming College of Health Sciences, Laramie, WY 82071, USA.
Maolong Dong
Yingmei Zhang
Feng Dong
Subat Turdi
Sreejayan Nair
Masashi Yanagisawa
Jun Ren
University of Wyoming · USAir Force Medical University · CNHoward Hughes Medical Institute · US

Funding

Wyoming INBRE Phase 4- Equipment Supplement for x-ray diffractometer for Center for Advanced Scientific InstrumentationP20GM103432 · NIGMS · UNIVERSITY OF WYOMING · PI Robert Scott Seville · 2012 to 2026
$56.8M
Wyoming IDeA Networks of Biomedical Research ExcellenceP20RR016474 · NCRR · UNIVERSITY OF WYOMING · PI LIBERLES, DAVID A. · 2001 to 2011
$28.2M
NCRR NIH HHS P20 RR016474NIGMS NIH HHS P20 GM103432
6 · The paper itself

Abstract

Cardiac aging is manifested as cardiac remodeling and contractile dysfunction although precise mechanisms remain elusive. This study was designed to examine the role of endothelin-1 (ET-1) in aging-associated myocardial morphological and contractile defects. Echocardiographic and cardiomyocyte contractile properties were evaluated in young (5-6 months) and old (26-28 months) C57BL/6 wild-type and cardiomyocyte-specific ET(A) receptor knockout (ETAKO) mice. Cardiac ROS production and histology were examined. Our data revealed that ETAKO mice displayed an improved survival. Aging increased plasma levels of ET-1 and Ang II, compromised cardiac function (fractional shortening, cardiomyocyte peak shortening, maximal velocity of shortening/relengthening and prolonged relengthening) and intracellular Ca(2+) handling (reduced intracellular Ca(2+) release and decay), the effects of which with the exception of ET-1 and Ang II levels was improved by ETAKO. Histological examination displayed cardiomyocyte hypertrophy and interstitial fibrosis associated with cardiac remodeling in aged C57 mice, which were alleviated in ETAKO mice. Aging promoted ROS generation, protein damage, ER stress, upregulated GATA4, ANP, NFATc3 and the autophagosome cargo protein p62, downregulated intracellular Ca(2+) regulatory proteins SERCA2a and phospholamban as well as the autophagic markers Beclin-1, Atg7, Atg5 and LC3BII, which were ablated by ETAKO. ET-1 triggered a decrease in autophagy and increased hypertrophic markers in vitro, the effect of which were reversed by the ET(A) receptor antagonist BQ123 and the autophagy inducer rapamycin. Antagonism of ET(A), but not ET(B) receptor, rescued cardiac aging, which was negated by autophagy inhibition. Taken together, our data suggest that cardiac ET(A) receptor ablation protects against aging-associated myocardial remodeling and contractile dysfunction possibly through autophagy regulation.

Indexed as

AgingAnimalsAutophagyBlotting, WesternCalciumCardiomegalyEchocardiographyEndothelin-1MaleMiceMice, Inbred C57BLMice, KnockoutMyocardial ContractionMyocytes, CardiacReactive Oxygen SpeciesReceptor, Endothelin ACalciumEndothelin-1Reactive Oxygen SpeciesReceptor, Endothelin A

Identifiers

PMID23381122
PMCPMC3590116
OpenAlexW2050183926

What OpenQuestion holds

Textmetadata
LicenceTDM
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.