Evidence map›Paper›PMID 32848821›Full record

ReviewFrontiers in physiology2020

Arrhythmogenic Cardiomyopathy and Skeletal Muscle Dystrophies: Shared Histopathological Features and Pathogenic Mechanisms.

Shanshan Gao, Suet Nee Chen, Carlo Di Nardo, Raffaella Lombardi

Abstract readReview
In one paragraph

Review in Frontiers in physiology, 2020. 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. 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

4 authors.

Shanshan GaoDivision of Cardiology, Department of Medicine, University of Colorado, Aurora, CO, United States.
Suet Nee ChenDivision of Cardiology, Department of Medicine, University of Colorado, Aurora, CO, United States.
Carlo Di NardoDivision of Cardiology, Department of Advanced Biomedical Sciences, Federico II University of Naples, Naples, Italy.
Raffaella LombardiDivision of Cardiology, Department of Medicine, University of Colorado, Aurora, CO, United States.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arrhythmogenic cardiomyopathy (ACM) is a heritable cardiac disease characterized by fibrotic or fibrofatty myocardial replacement, associated with an increased risk of ventricular arrhythmias and sudden cardiac death. Originally described as a disease of the right ventricle, ACM is currently recognized as a biventricular entity, due to the increasing numbers of reports of predominant left ventricular or biventricular involvement. Research over the last 20 years has significantly advanced our knowledge of the etiology and pathogenesis of ACM. Several etiopathogenetic theories have been proposed; among them, the most attractive one is the dystrophic theory, based on the observation of similar histopathological features between ACM and skeletal muscle dystrophies (SMDs), such as progressive muscular degeneration, inflammation, and tissue replacement by fatty and fibrous tissue. This review will describe the pathophysiological and molecular similarities shared by ACM with SMDs.

Indexed as

arrhythmogenic cardiomyopathyfibroadiposisinflammationmolecular pathogenesisskeletal muscle dystrophies

Identifiers

PMID32848821
PMCPMC7406798

What OpenQuestion holds

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Registered trials

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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.