Evidence map›Paper›PMID 38884766›Full record

ArticleAdvances in experimental medicine and biology2024

Molecular Pathways and Animal Models of Cardiomyopathies.

Buyan-Ochir Orgil, Enkhsaikhan Purevjav

Abstract read
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In one paragraph

Article in Advances in experimental medicine and biology, 2024. 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. Review
  2. Article
  3. 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

2 authors.

Buyan-Ochir OrgilDepartment of Pediatrics, The Heart Institute, Division of Cardiology, University of Tennessee Health Science Center, Memphis, TN, USA.
Enkhsaikhan PurevjavDepartment of Pediatrics, The Heart Institute, Division of Cardiology, University of Tennessee Health Science Center, Memphis, TN, USA. epurevja@uthsc.edu.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cardiomyopathies are a heterogeneous group of disorders of the heart muscle that ultimately result in congestive heart failure. Rapid progress in genetics, molecular and cellular biology with breakthrough innovative genetic-engineering techniques, such as next-generation sequencing and multiomics platforms, stem cell reprogramming, as well as novel groundbreaking gene-editing systems over the past 25 years has greatly improved the understanding of pathogenic signaling pathways in inherited cardiomyopathies. This chapter will focus on intracellular and intercellular molecular signaling pathways that are activated by a genetic insult in cardiomyocytes to maintain tissue and organ level regulation and resultant cardiac remodeling in certain forms of cardiomyopathies. In addition, animal models of different clinical forms of human cardiomyopathies with their summaries of triggered key molecules and signaling pathways will be described.

Indexed as

CardiomyopathiesDisease Models, AnimalMyocytes, CardiacSignal TransductionAnimalsHumansCardiac compensatory mechanismsCardiac remodelingCardiomyocyteCardiomyopathy animal modelCommon final pathwayFailing heartFetal gene programInherited cardiomyopathyMutationPathogenic variant

Identifiers

PMID38884766

What OpenQuestion holds

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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.