Evidence map›Paper›PMID 28319834›Full record

ReviewCardiovascular pathology : the official journal of the Society for Cardiovascular Pathology

Molecular mechanisms in the pathogenesis of arrhythmogenic cardiomyopathy.

Jeffrey E Saffitz

Abstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Arrhythmogenic Cardiomyopathy: Molecular Insights for Improved Therapeutic Design.Journal of cardiovascular development and disease · 2020
    Review
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

1 author.

Jeffrey E SaffitzDepartment of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, USA. Electronic address: jsaffitz@bidmc.harvard.edu.

Funding

REGULATION OF MYOCARDIAL GAP JUNCTIONSR01HL050598 · NHLBI · WASHINGTON UNIVERSITY · PI SAFFITZ, JEFFREY E · 1995 to 2006
$2.3M
CX43 IN A GENETIC MODEL OF ALTERED MYOCARDIAL CONDUCTIONR01HL058507 · NHLBI · WASHINGTON UNIVERSITY · PI SAFFITZ, JEFFREY E · 1998 to 2004
$1.8M
Disease Mechanisms in ARVCR01HL102361 · NHLBI · BETH ISRAEL DEACONESS MEDICAL CENTER · PI SAFFITZ, JEFFREY E · 2010 to 2013
$1.7M
NHLBI NIH HHS R01 HL050598NHLBI NIH HHS R01 HL058507NHLBI NIH HHS R01 HL102361
6 · The paper itself

Abstract

The article is based on work presented in the Distinguished Achievement Award lecture at the Society for Cardiovascular Pathology meeting in Seattle, WA, in March 2016. It reviews our current understanding of mechanisms responsible for a highly arrhythmogenic, nonischemic cardiomyopathy. It highlights the armamentarium of powerful methods available to the experimental pathologist in efforts to define how complex cardiovascular diseases work. It concludes with acknowledgment of the need for a far more detailed approach as to how we categorize human disease, a task for which pathologists are especially well positioned.

Indexed as

AnimalsAnimals, Genetically ModifiedArrhythmogenic Right Ventricular DysplasiaDisease Models, AnimalGenotypeGlycogen Synthase Kinase 3 betaHumansIndolesIon ChannelsMaleimidesMouth MucosaMyocytes, CardiacPhenotypeProtein Kinase InhibitorsProtein TransportWnt Signaling PathwayGlycogen Synthase Kinase 3 betaIndolesIon ChannelsMaleimidesProtein Kinase InhibitorsSB 216763Arrhythmogenic cardiomyopathyBuccal mucosaDesmosomesGap junctionsIon channelsProtein traffickingZebrafish models

Identifiers

PMID28319834
PMCPMC5423831

What OpenQuestion holds

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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.