Evidence map›Paper›PMID 40357789›Full record

ReviewCurrent pharmaceutical design2026

Expanding the Potential of Gene Therapy for Duchenne Muscular Dystrophy.

Gyas Khan, Md Sadique Hussain

Abstract readReview
PubMed Publisher
In one paragraph

Review in Current pharmaceutical design, 2026. 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. 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.

Gyas KhanDepartment of Pharmacology and Toxicology, College of Pharmacy, Jazan University, Jazan, Saudi Arabia.ORCID 0000-0003-2695-7401
Md Sadique HussainUttaranchal Institute of Pharmaceutical Sciences, Uttaranchal University, Prem Nagar, Dehradun, Uttarakhand, 248007, India.ORCID 0000-0002-3554-1750

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a severe X-linked neuromuscular disorder caused by mutations in the DMD gene, leading to progressive muscle degeneration, loss of ambulation, cardiomyopathy, and early mortality. While advances in multidisciplinary care and pharmacological interventions, including corticosteroids and exon-skipping therapies, have improved patient outcomes, current treatments primarily provide symptomatic relief without addressing the underlying genetic defect. Gene therapy has emerged as a promising approach to modify disease progression, particularly through the use of adeno-associated virus (AAV)-mediated delivery of micro-dystrophin constructs. These truncated genes retain essential functional domains, enabling the restoration of dystrophin expression within the packaging limits of AAV vectors. Early-phase clinical trials have demonstrated encouraging safety profiles and transgene expression; however, challenges such as immune responses, variability in functional improvement, and long-term durability remain. Recent innovations, including optimized AAV capsids, immunomodulatory strategies, and genome editing technologies like CRISPR-Cas9, are actively being explored to overcome these barriers. Additionally, scalable vector manufacturing and the integration of real-world data are essential for broader clinical translation. This review synthesizes current advancements, clinical milestones, and future directions in gene therapy for DMD, emphasizing the need for precise dosing, long-term efficacy, and equitable access to fully realize the therapeutic potential of these evolving strategies.

Indexed as

Genetic TherapyMuscular Dystrophy, DuchenneAnimalsDependovirusDystrophinGenetic VectorsHumansDystrophinAAV Vectorsclinical trialsCRISPR-Cas9dystrophingene editingmicro-dystrophintransgene expression.

Identifiers

What Socratic 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 Socratic graph.