Evidence map›Paper›PMID 40522885›Full record

ArticleAmerican journal of physiology. Cell physiology2025

Inhibition of mitochondrial fission protein Drp1 ameliorates skeletal myopathy in the D2-mdx model of Duchenne muscular dystrophy.

H Grace Rosen, Nicolas J Berger, Shantel N Hodge, Atsutaro Fujishiro, Jared Lourie, Vrusti Kapadia, Tessa Duzz, Melissa A Linden, Eunbin Jee, Jonghan Kim and 2 more

Abstract read
In one paragraph

Article in American journal of physiology. Cell physiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Article
  2. Review
  3. Review
  4. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

H Grace RosenDepartment of Biology, University of Massachusetts Boston, Boston, Massachusetts, United States.
Nicolas J BergerDepartment of Exercise and Health Sciences, University of Massachusetts Boston, Boston, Massachusetts, United States.
Shantel N HodgeDepartment of Biology, University of Massachusetts Boston, Boston, Massachusetts, United States.
Atsutaro FujishiroDepartment of Exercise and Health Sciences, University of Massachusetts Boston, Boston, Massachusetts, United States.
Jared LourieDepartment of Exercise and Health Sciences, University of Massachusetts Boston, Boston, Massachusetts, United States.ORCID 0009-0009-7169-4816
Vrusti KapadiaDepartment of Biology, University of Massachusetts Boston, Boston, Massachusetts, United States.
Tessa DuzzDepartment of Biology, University of Massachusetts Boston, Boston, Massachusetts, United States.
Melissa A LindenDepartment of Exercise and Health Sciences, University of Massachusetts Boston, Boston, Massachusetts, United States.ORCID 0000-0002-3152-0864
Eunbin JeeDepartment of Biomedical and Nutritional Sciences, University of Massachusetts Lowell, Lowell, Massachusetts, United States.
Jonghan KimDepartment of Biomedical and Nutritional Sciences, University of Massachusetts Lowell, Lowell, Massachusetts, United States.
Yuho KimDepartment of Physical Therapy and Kinesiology, University of Massachusetts Lowell, Lowell, Massachusetts, United States.ORCID 0000-0001-6038-4358
Kai ZouDepartment of Exercise and Health Sciences, University of Massachusetts Boston, Boston, Massachusetts, United States.ORCID 0000-0003-4164-7129

Funding

Transmission Electron Microscope for Core EM FacilityS10OD025113 · OD · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI HENDRICKS, GREGORY · 2018 to 2018
$600k
Targeting Dynamin-related protein 1-mediated mitochondrial fission to correct insulin resistance in obesityR15DK131512 · NIDDK · UNIVERSITY OF MASSACHUSETTS BOSTON · PI ZOU, KAI · 2021 to 2021
$456k
HHS | National Institutes of Health (NIH) S10 OD025113-01HHS | NIH | NIDDK | Division of Diabetes, Endocrinology, and Metabolic Diseases (DEM) R15DK131512NIDDK NIH HHS R15 DK131512NIH HHS S10 OD025113
6 · The paper itself

Abstract

Although current treatments for Duchenne muscular dystrophy (DMD) have proven to be effective in delaying myopathy, there remains a strong need to identify novel targets to develop additional therapies. Mitochondrial dysfunction is an early pathological feature of DMD. A fine balance of mitochondrial dynamics (fission and fusion) is crucial to maintain mitochondrial function and skeletal muscle health. Excessive activation of dynamin-related protein 1 (Drp1)-mediated mitochondrial fission was reported in animal models of DMD. However, whether Drp1-mediated mitochondrial fission is a viable target for treating myopathy in DMD remains unknown. Here, we treated a D2.B10-

Indexed as

DynaminsMitochondrial DynamicsMitochondria, MuscleMuscle, SkeletalMuscular Dystrophy, DuchenneQuinazolinonesAnimalsDisease Models, AnimalMaleMiceMice, Inbred mdxOxidative Stress3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinoneDnm1l protein, mouseDynaminsQuinazolinonesDrp1lipid peroxidationmitochondria dynamicsmusclemuscular dystrophy

Identifiers

PMID40522885
PMCPMC12291061

What Socratic holds

Textmetadata
LicenceTDM
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.