Evidence map›Paper›PMID 26055788›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2015

Attenuation of the unfolded protein response and endoplasmic reticulum stress after mechanical unloading in dilated cardiomyopathy.

Estibaliz Castillero, Hirokazu Akashi, Klara Pendrak, Halit Yerebakan, Marc Najjar, Catherine Wang, Yoshifumi Naka, Donna Mancini, H Lee Sweeney, Jeanine D Armiento and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed, 2 pooled it
3.3field-weighted citation impact, top 8% 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

35 citing papers in PubMed, 2 syntheses or guidelines pooled it, 53 citations in OpenAlex.

  1. Pooled it
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  12. Intensive stretch-activated CRT-PMCA1 feedback loop promoted apoptosis of myoblasts through CaApoptosis : an international journal on programmed cell death · 2022
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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

13 authors at 3 institutions in 1 country.

Estibaliz CastilleroDivision of Cardiothoracic Surgery, New York Presbyterian Hospital - College of Physicians and Surgeons of Columbia University, New York, New York;
Hirokazu AkashiDivision of Cardiothoracic Surgery, New York Presbyterian Hospital - College of Physicians and Surgeons of Columbia University, New York, New York;
Klara PendrakDepartment of Physiology, University of Pennsylvania, Philadelphia, Pennsylvania;
Halit YerebakanDivision of Cardiothoracic Surgery, New York Presbyterian Hospital - College of Physicians and Surgeons of Columbia University, New York, New York;
Marc NajjarDivision of Cardiothoracic Surgery, New York Presbyterian Hospital - College of Physicians and Surgeons of Columbia University, New York, New York;
Catherine WangDivision of Cardiothoracic Surgery, New York Presbyterian Hospital - College of Physicians and Surgeons of Columbia University, New York, New York;
Yoshifumi NakaDivision of Cardiothoracic Surgery, New York Presbyterian Hospital - College of Physicians and Surgeons of Columbia University, New York, New York;
Donna ManciniDivision of Cardiology, New York Presbyterian Hospital - College of Physicians and Surgeons of Columbia University, New York, New York; and.
H Lee SweeneyDepartment of Physiology, University of Pennsylvania, Philadelphia, Pennsylvania;
Jeanine D ArmientoDepartment of Anesthesiology, Physiology and Cellular Biophysics, College of Physicians and Surgeons of Columbia University, New York, New York.
Ziad A AliDivision of Cardiology, New York Presbyterian Hospital - College of Physicians and Surgeons of Columbia University, New York, New York; and.
P Christian SchulzeDivision of Cardiology, New York Presbyterian Hospital - College of Physicians and Surgeons of Columbia University, New York, New York; and.
Isaac GeorgeDivision of Cardiothoracic Surgery, New York Presbyterian Hospital - College of Physicians and Surgeons of Columbia University, New York, New York; ig2006@cumc.columbia.edu.
Columbia University · USNewYork–Presbyterian Hospital · USUniversity of Pennsylvania · US

Funding

CTSA INFRASTRUCTURE FOR PEDIATRIC RESEARCHUL1RR024156 · NCRR · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2006 to 2011
$53.0M
Clinical and Translational Science AwardUL1TR000040 · NCATS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI GINSBERG, HENRY N · 2012 to 2015
$26.2M
Cardiac Lipotoxicity and Ceramide Metabolism in Heart FailureR01HL114813 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI COLOMBO, PAOLO C, SCHULZE, P. CHRISTIAN · 2013 to 2017
$3.0M
NCATS NIH HHS UL1 TR000040NCRR NIH HHS RR024156NHLBI NIH HHS R01 HL114813
6 · The paper itself

Abstract

Abnormal intracellular calcium (Ca(2+)) handling can trigger endoplasmic reticulum (ER) stress, leading to activation of the unfolded protein response (UPR) in an attempt to prevent cell death. Mechanical unloading with a left ventricular assist device (LVAD) relieves pressure-volume overload and promotes reverse remodeling of the failing myocardium. We hypothesized that mechanical unloading would alter the UPR in patients with advanced heart failure (HF). UPR was analyzed in paired myocardial tissue from 10 patients with dilated cardiomyopathy obtained during LVAD implantation and explantation. Samples from healthy hearts served as controls. Markers of UPR [binding immunoglobulin protein (BiP), phosphorylated (P-) eukaryotic initiation factor (eIF2α), and X-box binding protein (XBP1)] were significantly increased in HF, whereas LVAD support significantly decreased BiP, P-eIF2α, and XBP1s levels. Apoptosis as reflected by C/EBP homologous protein and DNA damage were also significantly reduced after LVAD support. Improvement in left ventricular dimensions positively correlated with P-eIF2α/eIF2α and apoptosis level recovery. Furthermore, significant dysregulation of calcium-handling proteins [P-ryanodine receptor, Ca(2+) storing protein calsequestrin, Na(+)-Ca(2+) exchanger, sarcoendoplasmic reticulum Ca(2+)-ATPase (SERCA2a), ER chaperone protein calreticulin] was normalized after LVAD support. Reduced ER Ca(2+) content as a causative mechanism for UPR was confirmed using AC16 cells treated with a calcium ionophore (A23187) and SERCA2a inhibitor (thapsigargin). UPR activation and apoptosis are reduced after mechanical unloading, which may be mediated by the improvement of Ca(2+) handling in patients with advanced HF. These changes may impact the potential for myocardial recovery.

Indexed as

Endoplasmic Reticulum StressHeart-Assist DevicesUnfolded Protein ResponseApoptosisCalreticulinCardiomyopathy, DilatedCase-Control StudiesCell LineDNA-Binding ProteinseIF-2 KinaseFemaleHeart VentriclesHumansMaleMiddle AgedRegulatory Factor X Transcription FactorsCalreticulinDNA-Binding ProteinseIF-2 KinaseRegulatory Factor X Transcription FactorsRyanodine Receptor Calcium Release ChannelSarcoplasmic Reticulum Calcium-Transporting ATPasesTranscription FactorsX-Box Binding Protein 1XBP1 protein, humanendoplasmic reticulum stressunfolded protein responseventricular assist device

Identifiers

PMID26055788
PMCPMC4525088
OpenAlexW1886829050

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.