Evidence map›Paper›PMID 23464837›Full record

ArticleBioscience reports2013

Knockdown of cathepsin D in zebrafish fertilized eggs determines congenital myopathy.

Carlo Follo, Matteo Ozzano, Claudia Montalenti, Massimo Mattia Santoro, Ciro Isidoro

Open access · goldAbstract read
In one paragraph

Article in Bioscience reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

13 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Genes · 2022
    Article
  3. Review
  4. Article
  5. Article
  6. Modeling Lysosomal Storage Diseases in the Zebrafish.Frontiers in molecular biosciences · 2020
    Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Modelling inborn errors of metabolism in zebrafish.Journal of inherited metabolic disease · 2014
    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

5 authors at 2 institutions in 1 country.

Carlo Follo*Laboratorio di Patologia Molecolare, Dipartimento di Scienze della Salute dell'Università del Piemonte Orientale, Via Solaroli 17, 28100 Novara, Italy.
Matteo Ozzano*Laboratorio di Patologia Molecolare, Dipartimento di Scienze della Salute dell'Università del Piemonte Orientale, Via Solaroli 17, 28100 Novara, Italy.
Claudia Montalenti*Laboratorio di Patologia Molecolare, Dipartimento di Scienze della Salute dell'Università del Piemonte Orientale, Via Solaroli 17, 28100 Novara, Italy.
Massimo Mattia Santoro†Department of Molecular Biotechnology and Health Sciences, Molecular Biotechnology Center, University of Torino, Via Nizza, 52, 10126 Torino, Italy.
Ciro Isidoro*Laboratorio di Patologia Molecolare, Dipartimento di Scienze della Salute dell'Università del Piemonte Orientale, Via Solaroli 17, 28100 Novara, Italy.
Università degli Studi del Piemonte Orientale “Amedeo Avogadro” · ITUniversity of Turin · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

CD (cathepsin D) is a ubiquitous lysosomal hydrolase involved in a variety of pathophysiological functions, including protein turnover, activation of pro-hormones, cell death and embryo development. CD-mediated proteolysis plays a pivotal role in tissue and organ homoeostasis. Altered expression and compartmentalization of CD have been observed in diseased muscle fibres. Whether CD is actively involved in muscle development, homoeostasis and dystrophy remains to be demonstrated. Zebrafish (Danio rerio) is emerging as a valuable 'in vivo' vertebrate model for muscular degeneration and congenital myopathies. In this work, we report on the perturbance of the somitic musculature development in zebrafish larvae caused by MPO (morpholino)-mediated silencing of CD in oocytes at the time of fertilization. Restoring CD expression, using an MPO-non-matching mutated mRNA, partially rescued the normal phenotype, confirming the indispensable role of CD in the correct development and integrity of the somitic musculature. This is the first report showing a congenital myopathy caused by CD deficiency in a vertebrate experimental animal model.

Indexed as

AnimalsCathepsin DDisease Models, AnimalGene Expression Regulation, DevelopmentalGene Knockdown TechniquesGene SilencingHumansMyopathies, Structural, CongenitalRNA, MessengerZebrafishZygoteCathepsin DRNA, Messenger

Identifiers

PMID23464837
PMCPMC3616520
OpenAlexW2021843856

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.