Evidence map›Paper›PMID 40955317›Full record

ArticleMolecular therapy. Methods & clinical development2025

Nanoparticle delivery of AMPK activator 991 prevents its toxicity and improves muscle homeostasis in Duchenne muscular dystrophy.

Ilaria Andreana, Ananga Ghosh, Mathieu Repellin, Anita Kneppers, Sabrina Ben Larbi, Federica Tifni, Aurélie Fessard, Marion Martin, Jacqueline Sidi-Boumedine, David Kryza and 9 more

Abstract read
In one paragraph

Article in Molecular therapy. Methods & clinical development, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Review
  2. Review
  3. 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

19 authors.

Ilaria AndreanaDipartimento di Scienza e Tecnologia del Farmaco, Università di Torino, Torino, Italy.
Ananga GhoshInstitut NeuroMyoGène, Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, Inserm U1315, CNRS UMR 5261, Université de Lyon, Lyon, France.
Mathieu RepellinLaboratoire d'Automatique, de Génie des Procédés et de Génie Pharmaceutique, Université Claude Bernard Lyon 1, CNRS UMR 5007, Villeurbanne, France.
Anita KneppersInstitut NeuroMyoGène, Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, Inserm U1315, CNRS UMR 5261, Université de Lyon, Lyon, France.
Sabrina Ben LarbiInstitut NeuroMyoGène, Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, Inserm U1315, CNRS UMR 5261, Université de Lyon, Lyon, France.
Federica TifniDipartimento di Scienza e Tecnologia del Farmaco, Università di Torino, Torino, Italy.
Aurélie FessardInstitut NeuroMyoGène, Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, Inserm U1315, CNRS UMR 5261, Université de Lyon, Lyon, France.
Marion MartinInstitut NeuroMyoGène, Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, Inserm U1315, CNRS UMR 5261, Université de Lyon, Lyon, France.
Jacqueline Sidi-BoumedineLaboratoire d'Automatique, de Génie des Procédés et de Génie Pharmaceutique, Université Claude Bernard Lyon 1, CNRS UMR 5007, Villeurbanne, France.
David KryzaLaboratoire d'Automatique, de Génie des Procédés et de Génie Pharmaceutique, Université Claude Bernard Lyon 1, CNRS UMR 5007, Villeurbanne, France.
Barbara StellaDipartimento di Scienza e Tecnologia del Farmaco, Università di Torino, Torino, Italy.
Silvia ArpiccoDipartimento di Scienza e Tecnologia del Farmaco, Università di Torino, Torino, Italy.
Claire BordesLaboratoire d'Automatique, de Génie des Procédés et de Génie Pharmaceutique, Université Claude Bernard Lyon 1, CNRS UMR 5007, Villeurbanne, France.
Yves ChevalierLaboratoire d'Automatique, de Génie des Procédés et de Génie Pharmaceutique, Université Claude Bernard Lyon 1, CNRS UMR 5007, Villeurbanne, France.
Julien GondinInstitut NeuroMyoGène, Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, Inserm U1315, CNRS UMR 5261, Université de Lyon, Lyon, France.
Bénédicte ChazaudInstitut NeuroMyoGène, Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, Inserm U1315, CNRS UMR 5261, Université de Lyon, Lyon, France.
Rémi MounierInstitut NeuroMyoGène, Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, Inserm U1315, CNRS UMR 5261, Université de Lyon, Lyon, France.
Giovanna LolloLaboratoire d'Automatique, de Génie des Procédés et de Génie Pharmaceutique, Université Claude Bernard Lyon 1, CNRS UMR 5007, Villeurbanne, France.
Gaëtan JubanInstitut NeuroMyoGène, Physiopathologie et Génétique du Neurone et du Muscle, Université Claude Bernard Lyon 1, Inserm U1315, CNRS UMR 5261, Université de Lyon, Lyon, France.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Muscular dystrophies, such as Duchenne muscular dystrophy (DMD), are caused by permanent muscle injuries leading to chronic inflammation, with macrophages harboring an altered inflammatory profile contributing to fibrosis through the secretion of transforming growth factor β1 (TGF-β1). We previously showed that AMP-activated protein kinase (AMPK) activation reduces TGF-β1 secretion by macrophages and improves muscle homeostasis and muscle force in a DMD mouse model. However, direct AMPK activators like compound 991 show strong adverse effects

Indexed as

AMPKchronic inflammationDuchenne muscular dystrophyfibrosisPLGA nanoparticles

Identifiers

PMID40955317
PMCPMC12433517

What Socratic 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 Socratic graph.