Evidence map›Paper›PMID 37917377›Full record

ReviewBioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy2024

Dystrophin- and Utrophin-Based Therapeutic Approaches for Treatment of Duchenne Muscular Dystrophy: A Comparative Review.

Sylwia Szwec, Zuzanna Kapłucha, Jeffrey S Chamberlain, Patryk Konieczny

Erratum issuedOpen access · hybridAbstract readComparative StudyReview
In one paragraph

Review in BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Article
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  4. Review
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  10. Biallelic variants in theFrontiers in genetics · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Sylwia SzwecInstitute of Human Biology and Evolution, Faculty of Biology, Adam Mickiewicz University, ul. Uniwersytetu Poznańskiego 6, 61-614, Poznań, Poland.
Zuzanna KapłuchaInstitute of Human Biology and Evolution, Faculty of Biology, Adam Mickiewicz University, ul. Uniwersytetu Poznańskiego 6, 61-614, Poznań, Poland.
Jeffrey S ChamberlainDepartment of Neurology, University of Washington School of Medicine, Seattle, WA, 98109-8055, USA.
Patryk KoniecznyInstitute of Human Biology and Evolution, Faculty of Biology, Adam Mickiewicz University, ul. Uniwersytetu Poznańskiego 6, 61-614, Poznań, Poland. patryk.konieczny@amu.edu.pl.ORCID http://orcid.org/0000-0002-9609-8254
Adam Mickiewicz University in Poznań · PLUniversity of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Karin E Bornfeldt · 1986 to 2026
$41.4M
Wellstone Muscular Dystrophy Specialized Research Center (Seattle)P50AR065139 · NIAMS · UNIVERSITY OF WASHINGTON · PI JEFFREY S CHAMBERLAIN · 2018 to 2026
$15.9M
DYSTROPHIN REPLACEMENT IN MDX MICER01AR040864 · NIAMS · UNIVERSITY OF WASHINGTON · PI JEFFREY S CHAMBERLAIN · 1991 to 2026
$8.8M
NIAMS NIH HHS P50 AR065139NIAMS NIH HHS R01 AR040864NIDDK NIH HHS P30 DK017047
6 · The paper itself

Abstract

Duchenne muscular dystrophy is a devastating disease that leads to progressive muscle loss and premature death. While medical management focuses mostly on symptomatic treatment, decades of research have resulted in first therapeutics able to restore the affected reading frame of dystrophin transcripts or induce synthesis of a truncated dystrophin protein from a vector, with other strategies based on gene therapy and cell signaling in preclinical or clinical development. Nevertheless, recent reports show that potentially therapeutic dystrophins can be immunogenic in patients. This raises the question of whether a dystrophin paralog, utrophin, could be a more suitable therapeutic protein. Here, we compare dystrophin and utrophin amino acid sequences and structures, combining published data with our extended in silico analyses. We then discuss these results in the context of therapeutic approaches for Duchenne muscular dystrophy. Specifically, we focus on strategies based on delivery of micro-dystrophin and micro-utrophin genes with recombinant adeno-associated viral vectors, exon skipping of the mutated dystrophin pre-mRNAs, reading through termination codons with small molecules that mask premature stop codons, dystrophin gene repair by clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated protein 9 (CRISPR/Cas9)-mediated genetic engineering, and increasing utrophin levels. Our analyses highlight the importance of various dystrophin and utrophin domains in Duchenne muscular dystrophy treatment, providing insights into designing novel therapeutic compounds with improved efficacy and decreased immunoreactivity. While the necessary actin and β-dystroglycan binding sites are present in both proteins, important functional distinctions can be identified in these domains and some other parts of truncated dystrophins might need redesigning due to their potentially immunogenic qualities. Alternatively, therapies based on utrophins might provide a safer and more effective approach.

Indexed as

DystrophinMuscular Dystrophy, DuchenneGenetic TherapyHumansUtrophinDystrophinUtrophin

Identifiers

PMID37917377
PMCPMC10789850
OpenAlexW4388222534

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.