Evidence map›Paper›PMID 23437120›Full record

ArticlePloS one2013

Calreticulin induces dilated cardiomyopathy.

Dukgyu Lee, Tatsujiro Oka, Beth Hunter, Alison Robinson, Sylvia Papp, Kimitoshi Nakamura, Wattamon Srisakuldee, Barbara E Nickel, Peter E Light, Jason R B Dyck and 4 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

16 citing papers in PubMed, 31 citations in OpenAlex.

  1. Review
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  8. Stress Coping Strategies in the Heart: An Integrated View.Frontiers in cardiovascular medicine · 2018
    Review
  9. Activation of theDisease models & mechanisms · 2017
    Article
  10. Article
  11. The Mutation Profile of Calreticulin in Patients with Myeloproliferative Neoplasms and Acute Leukemia.Turkish journal of haematology : official journal of Turkish Society of Haematology · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. The role of heat shock proteins in atherosclerosis.Nature reviews. Cardiology · 2014
    Review
  16. Article
4 · The record

Corrections and comments

  • Erratum issued
5 · Who and what money

Authors and funding

14 authors at 5 institutions in 2 countries.

Dukgyu LeeDepartment of Biochemistry, University of Alberta, Edmonton, Alberta, Canada.
Tatsujiro Oka
Beth Hunter
Alison Robinson
Sylvia Papp
Kimitoshi Nakamura
Wattamon Srisakuldee
Barbara E Nickel
Peter E Light
Jason R B Dyck
Gary D Lopaschuk
Elissavet Kardami
Michal Opas
Marek Michalak
University of Alberta · CAUniversity of Manitoba · CAUniversity of Toronto · CAKumamoto University · JPSt. Boniface Hospital · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

backgroundCalreticulin, a Ca(2+)-buffering chaperone of the endoplasmic reticulum, is highly expressed in the embryonic heart and is essential for cardiac development. After birth, the calreticulin gene is sharply down regulated in the heart, and thus, adult hearts have negligible levels of calreticulin. In this study we tested the role of calreticulin in the adult heart. METHODOLOGY/PRINCIPAL

findingsWe generated an inducible transgenic mouse in which calreticulin is targeted to the cardiac tissue using a Cre/loxP system and can be up-regulated in adult hearts. Echocardiography analysis of hearts from transgenic mice expressing calreticulin revealed impaired left ventricular systolic and diastolic function and impaired mitral valve function. There was altered expression of Ca(2+) signaling molecules and the gap junction proteins, Connexin 43 and 45. Sarcoplasmic reticulum associated Ca(2+)-handling proteins (including the cardiac ryanodine receptor, sarco/endoplasmic reticulum Ca(2+)-ATPase, and cardiac calsequestrin) were down-regulated in the transgenic hearts with increased expression of calreticulin. CONCLUSIONS/SIGNIFICANCE: We show that in adult heart, up-regulated expression of calreticulin induces cardiomyopathy in vivo leading to heart failure. This is due to an alternation in changes in a subset of Ca(2+) handling genes, gap junction components and left ventricle remodeling.

Indexed as

AnimalsCalcium SignalingCalreticulinCalsequestrinCardiomyopathy, DilatedChickensConnexinsDown-RegulationElectrocardiographyMiceMice, Inbred C57BLMice, TransgenicMyocardiumMyosin Heavy ChainsOrgan SpecificityPromoter Regions, GeneticCalreticulinCalsequestrinConnexinsMyosin Heavy ChainsRNA, Messenger

Identifiers

PMID23437120
PMCPMC3577809
OpenAlexW2032647451

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.