Evidence map›Paper›PMID 26050991›Full record

ArticleMolecular therapy : the journal of the American Society of Gene Therapy2015

Galectin-1 Protein Therapy Prevents Pathology and Improves Muscle Function in the mdx Mouse Model of Duchenne Muscular Dystrophy.

Pam M Van Ry, Ryan D Wuebbles, Megan Key, Dean J Burkin

Open access · bronzeAbstract read
In one paragraph

Article in Molecular therapy : the journal of the American Society of Gene Therapy, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 41 citations in OpenAlex.

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  11. PDE10A Inhibition Reduces the Manifestation of Pathology in DMD Zebrafish and Represses the Genetic Modifier PITPNA.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
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  17. Slow-twitch skeletal muscle defects accompany cardiac dysfunction in transgenic mice with a mutation in the myosin regulatory light chain.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019
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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

4 authors at 1 institution in 1 country.

Pam M Van RyDepartment of Pharmacology, University of Nevada School of Medicine, Reno, Nevada, USA.
Ryan D WuebblesDepartment of Pharmacology, University of Nevada School of Medicine, Reno, Nevada, USA.
Megan KeyDepartment of Pharmacology, University of Nevada School of Medicine, Reno, Nevada, USA.
Dean J BurkinDepartment of Pharmacology, University of Nevada School of Medicine, Reno, Nevada, USA. Electronic address: dburkin@medicine.nevada.edu.
University of Nevada, Reno · US

Funding

Laminin protein therapy for Congenital Muscular DystrophyR01AR064338 · NIAMS · UNIVERSITY OF NEVADA RENO · PI BURKIN, DEAN J. · 2014 to 2018
$1.6M
Integrin Alleviation of Muscular DystrophyR01AR053697 · NIAMS · UNIVERSITY OF NEVADA RENO · PI BURKIN, DEAN J. · 2008 to 2012
$1.2M
Galectin 1: A novel small protein therapy for Duchenne muscular dystrophyR41AR067014 · NIAMS · STRYKAGEN CORPORATION · PI BURKIN, DEAN J. · 2014 to 2015
$225k
NIAMS NIH HHS R01 AR053697NIAMS NIH HHS R01AR053697NIAMS NIH HHS R01 AR064338NIAMS NIH HHS R01AR064338NIAMS NIH HHS R41 AR067014NIAMS NIH HHS R41AR067014
6 · The paper itself

Abstract

Duchenne muscular dystrophy (DMD) is a fatal neuromuscular disease caused by mutations in the dystrophin gene, leading to the loss of a critical component of the sarcolemmal dystrophin glycoprotein complex. Galectin-1 is a small 14 kDa protein normally found in skeletal muscle and has been shown to be a modifier of immune response, muscle repair, and apoptosis. Galectin-1 levels are elevated in the muscle of mouse and dog models of DMD. Together, these findings led us to hypothesize that Galectin-1 may serve as a modifier of disease progression in DMD. To test this hypothesis, recombinant mouse Galectin-1 was produced and used to treat myogenic cells and the mdx mouse model of DMD. Here we show that intramuscular and intraperitoneal injections of Galectin-1 into mdx mice prevented pathology and improved muscle function in skeletal muscle. These improvements were a result of enhanced sarcolemmal stability mediated by elevated utrophin and α7β1 integrin protein levels. Together our results demonstrate for the first time that Galectin-1 may serve as an exciting new protein therapeutic for the treatment of DMD.

Indexed as

AnimalsCell LineDisease Models, AnimalDystroglycansExtracellular MatrixGalectin 1HumansIntegrinsMiceMice, Inbred mdxMuscle, SkeletalMuscular Dystrophy, DuchenneRecombinant ProteinsSarcolemmaUtrophinDystroglycansGalectin 1integrin alpha7beta1IntegrinsLGALS1 protein, humanRecombinant ProteinsUtrophin

Identifiers

PMID26050991
PMCPMC4817863
OpenAlexW1512137762

What OpenQuestion 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 OpenQuestion graph.