Evidence map›Paper›PMID 24877152›Full record

ReviewBioMed research international2014

Understanding the process of fibrosis in Duchenne muscular dystrophy.

Yacine Kharraz, Joana Guerra, Patrizia Pessina, Antonio L Serrano, Pura Muñoz-Cánoves

Registry-linked trialOpen access · hybridAbstract readReview
In one paragraph

Review in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT05637216 (A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients), which is not on this map. Cited by 164 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
164citing papers in PubMed, 2 pooled it
7.8field-weighted citation impact, top 2% 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.

NCT05637216 phase2active not recruitingnot on this mapstarted 2023, after this paper: background citation

A Pilot Study of Losartan to Reduce Radiation Induced Fibrosis in Breast Cancer Patients

TypeinterventionalSponsorShaw Cancer CenterRan2023 to 2027Enrolled43ConditionsRadiation Induced FibrosisArmsLosartan 25 milligram capsule, Placebo
3 · Its place in the literature

Who cites it

164 citing papers in PubMed, 2 syntheses or guidelines pooled it, 249 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Trial
  4. Viltolarsen in Japanese Duchenne muscular dystrophy patients: A phase 1/2 study.Annals of clinical and translational neurology · 2020
    Trial
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104 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Yacine KharrazCell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University (UPF), CIBER on Neurodegenerative diseases (CIBERNED), Institució Catalana de Recerca i Estudis Avançats (ICREA), Doctor Aiguader 83, 08003 Barcelona, Spain.
Joana GuerraCell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University (UPF), CIBER on Neurodegenerative diseases (CIBERNED), Institució Catalana de Recerca i Estudis Avançats (ICREA), Doctor Aiguader 83, 08003 Barcelona, Spain.
Patrizia PessinaCell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University (UPF), CIBER on Neurodegenerative diseases (CIBERNED), Institució Catalana de Recerca i Estudis Avançats (ICREA), Doctor Aiguader 83, 08003 Barcelona, Spain.ORCID 0000-0002-4227-411X
Antonio L SerranoCell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University (UPF), CIBER on Neurodegenerative diseases (CIBERNED), Institució Catalana de Recerca i Estudis Avançats (ICREA), Doctor Aiguader 83, 08003 Barcelona, Spain.
Pura Muñoz-CánovesCell Biology Group, Department of Experimental and Health Sciences, Pompeu Fabra University (UPF), CIBER on Neurodegenerative diseases (CIBERNED), Institució Catalana de Recerca i Estudis Avançats (ICREA), Doctor Aiguader 83, 08003 Barcelona, Spain.
Institució Catalana de Recerca i Estudis Avançats · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Fibrosis is the aberrant deposition of extracellular matrix (ECM) components during tissue healing leading to loss of its architecture and function. Fibrotic diseases are often associated with chronic pathologies and occur in a large variety of vital organs and tissues, including skeletal muscle. In human muscle, fibrosis is most readily associated with the severe muscle wasting disorder Duchenne muscular dystrophy (DMD), caused by loss of dystrophin gene function. In DMD, skeletal muscle degenerates and is infiltrated by inflammatory cells and the functions of the muscle stem cells (satellite cells) become impeded and fibrogenic cells hyperproliferate and are overactivated, leading to the substitution of skeletal muscle with nonfunctional fibrotic tissue. Here, we review new developments in our understanding of the mechanisms leading to fibrosis in DMD and several recent advances towards reverting it, as potential treatments to attenuate disease progression.

Indexed as

AnimalsDystrophinFibrosisHumansMuscle, SkeletalMuscular Dystrophy, DuchenneSatellite Cells, Skeletal MuscleDystrophin

Identifiers

PMID24877152
PMCPMC4024417
OpenAlexW2172191780

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

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.