Evidence map›Paper›PMID 25332179›Full record

ArticleJournal of the American Heart Association2014

Endoplasmic reticulum resident protein 44 (ERp44) deficiency in mice and zebrafish leads to cardiac developmental and functional defects.

Ding-Yan Wang, Cynthia Abbasi, Suzan El-Rass, Jamie Yuanjun Li, Fayez Dawood, Kotaro Naito, Parveen Sharma, Nicolas Bousette, Shalini Singh, Peter H Backx and 4 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of the American Heart Association, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

14 citing papers in PubMed, 30 citations in OpenAlex.

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  7. ER stress and calcium-dependent arrhythmias.Frontiers in physiology · 2022
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  9. IP3R1 regulates CaCell death discovery · 2021
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  13. Review
  14. Resolving Myocardial Activation With Novel Omnipolar Electrograms.Circulation. Arrhythmia and electrophysiology · 2016
    Article
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

14 authors at 2 institutions in 1 country.

Ding-Yan WangDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.).
Cynthia AbbasiDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.).
Suzan El-RassFaculty of Medicine and Institute of Medical Science, University of Toronto, Ontario, Canada (S.E.R., F.D., K.N., P.H.B., X.Y.W., P.P.L., A.O.G.) Keenan Research Center for Biomedical Science and Zebrafish Center for Advanced Drug Discovery, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada (S.E.R., X.Y.W.).
Jamie Yuanjun LiDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.).
Fayez DawoodFaculty of Medicine and Institute of Medical Science, University of Toronto, Ontario, Canada (S.E.R., F.D., K.N., P.H.B., X.Y.W., P.P.L., A.O.G.).
Kotaro NaitoFaculty of Medicine and Institute of Medical Science, University of Toronto, Ontario, Canada (S.E.R., F.D., K.N., P.H.B., X.Y.W., P.P.L., A.O.G.).
Parveen SharmaDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.).
Nicolas BousetteDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.).
Shalini SinghDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.).
Peter H BackxDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.) Faculty of Medicine and Institute of Medical Science, University of Toronto, Ontario, Canada (S.E.R., F.D., K.N., P.H.B., X.Y.W., P.P.L., A.O.G.).
Brian CoxDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.).
Xiao-Yan WenDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.) Faculty of Medicine and Institute of Medical Science, University of Toronto, Ontario, Canada (S.E.R., F.D., K.N., P.H.B., X.Y.W., P.P.L., A.O.G.) Keenan Research Center for Biomedical Science and Zebrafish Center for Advanced Drug Discovery, Li Ka Shing Knowledge Institute, St. Michael's Hospital, Toronto, Ontario, Canada (S.E.R., X.Y.W.).
Peter P LiuDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.) Faculty of Medicine and Institute of Medical Science, University of Toronto, Ontario, Canada (S.E.R., F.D., K.N., P.H.B., X.Y.W., P.P.L., A.O.G.).
Anthony O GramoliniDepartment of Physiology, University of Toronto, Ontario, Canada (D.Y.W., C.A., J.Y.L., P.S., N.B., S.S., P.H.B., B.C., X.Y.W., P.P.L., A.O.G.) Faculty of Medicine and Institute of Medical Science, University of Toronto, Ontario, Canada (S.E.R., F.D., K.N., P.H.B., X.Y.W., P.P.L., A.O.G.).
University of Toronto · CASt. Michael's Hospital · CA

Funding

Canadian Institutes of Health Research GPG-102166Canadian Institutes of Health Research MOP-106538
6 · The paper itself

Abstract

backgroundEndoplasmic reticulum (ER) resident protein 44 (ERp44) is a member of the protein disulfide isomerase family, is induced during ER stress, and may be involved in regulating Ca(2+) homeostasis. However, the role of ERp44 in cardiac development and function is unknown. The aim of this study was to investigate the role of ERp44 in cardiac development and function in mice, zebrafish, and embryonic stem cell (ESC)-derived cardiomyocytes to determine the underlying role of ERp44. METHODS AND

resultsWe generated and characterized ERp44(-/-) mice, ERp44 morphant zebrafish embryos, and ERp44(-/-) ESC-derived cardiomyocytes. Deletion of ERp44 in mouse and zebrafish caused significant embryonic lethality, abnormal heart development, altered Ca(2+) dynamics, reactive oxygen species generation, activated ER stress gene profiles, and apoptotic cell death. We also determined the cardiac phenotype in pressure overloaded, aortic-banded ERp44(+/-) mice: enhanced ER stress activation and increased mortality, as well as diastolic cardiac dysfunction with a significantly lower fractional shortening. Confocal and LacZ histochemical staining showed a significant transmural gradient for ERp44 in the adult heart, in which high expression of ERp44 was observed in the outer subepicardial region of the myocardium.

conclusionsERp44 plays a critical role in embryonic heart development and is crucial in regulating cardiac cell Ca(2+) signaling, ER stress, ROS-induced oxidative stress, and activation of the intrinsic mitochondrial apoptosis pathway.

Indexed as

AnimalsApoptosisCalcium SignalingCells, CulturedEmbryonic Stem CellsEndoplasmic ReticulumEndoplasmic Reticulum StressHeart Defects, CongenitalMembrane ProteinsMice, 129 StrainMice, Inbred C57BLMice, KnockoutMitochondria, HeartMolecular ChaperonesMorphogenesisMyocardial ContractionERp44 protein, mouseMembrane ProteinsMolecular ChaperonesReactive Oxygen SpeciesZebrafish ProteinsapoptosisCa2+ERp44−/−ESC‐derived cardiomyocytesheart development and cardiomyopathy

Identifiers

PMID25332179
PMCPMC4323785
OpenAlexW2156235806

What OpenQuestion holds

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LicenceCC BY-NC
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.