Evidence map›Paper›PMID 15360134›Full record

ArticleJournal of muscle research and cell motility2004

Function induced modifications of gene expression: an alternative approach to gene therapy of Duchenne muscular dystrophy.

Gerta Vrbová

Abstract read
PubMed Publisher
In one paragraph

Article in Journal of muscle research and cell motility, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

1 author.

Gerta VrbováDepartment of Anatomy and Developmental Biology, University College London, Gower Street, London WC1E 6BT, UK. g.vrbova@ucl.ac.uk

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In Duchenne muscular dystrophy a large gene that codes for dystrophin is altered. The possibility that the defective gene/protein could be at least in part substituted by other molecules that the diseased muscle is able to produce and that have a function similar to that of dystrophin is being discussed. Muscle fibres have a tremendous adaptive potential, and the expression of several protein isoforms can be induced by either stretch or long-term change of activity. The exploitation of this ability of muscle cells to express new genes, which would code for proteins that will not be alien to the individual, for treatment of Duchenne muscular dystrophy is being considered. The argument for this approach is strengthened by results that in patients with Duchenne muscular dystrophy the progress of the disease can be slowed with changes of muscle activity.

Indexed as

Gene Expression RegulationBiomechanical PhenomenaDystrophinElectric StimulationGenetic TherapyHumansIon ChannelsMuscle ContractionMuscle Fibers, SkeletalMuscular Dystrophy, DuchenneMyoblastsStem Cell TransplantationWeight-BearingDystrophinIon Channels

Identifiers

What OpenQuestion holds

Textmetadata
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.