Evidence map›Paper›PMID 39014470›Full record

ArticleJournal of translational medicine2024

Exploring lipin1 as a promising therapeutic target for the treatment of Duchenne muscular dystrophy.

Abdulrahman Jama, Abdullah A Alshudukhi, Steve Burke, Lixin Dong, John Karanja Kamau, Brooklyn Morris, Ibrahim A Alkhomsi, Brian N Finck, Andrew Alvin Voss, Hongmei Ren

Abstract read
In one paragraph

Article in Journal of translational medicine, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

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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

10 authors.

Abdulrahman Jama *Department of Biochemistry and Molecular Biology, Wright State University, 3640 Colonel Glenn Hwy., Dayton, OH, 45435-0001, USA.
Abdullah A Alshudukhi *Department of Biochemistry and Molecular Biology, Wright State University, 3640 Colonel Glenn Hwy., Dayton, OH, 45435-0001, USA.
Steve BurkeDepartment of Biological Sciences, Wright State University, Dayton, OH, USA.
Lixin DongMumetel LLC, University Technology Park at IIT, Chicago, IL, USA.
John Karanja KamauDepartment of Biochemistry and Molecular Biology, Wright State University, 3640 Colonel Glenn Hwy., Dayton, OH, 45435-0001, USA.
Brooklyn MorrisDepartment of Biochemistry and Molecular Biology, Wright State University, 3640 Colonel Glenn Hwy., Dayton, OH, 45435-0001, USA.
Ibrahim A AlkhomsiDepartment of Biochemistry and Molecular Biology, Wright State University, 3640 Colonel Glenn Hwy., Dayton, OH, 45435-0001, USA.
Brian N FinckDivision of Geriatrics & Nutritional Science, Washington University School of Medicine, St. Louis, USA.
Andrew Alvin VossDepartment of Biological Sciences, Wright State University, Dayton, OH, USA.
Hongmei RenDepartment of Biochemistry and Molecular Biology, Wright State University, 3640 Colonel Glenn Hwy., Dayton, OH, 45435-0001, USA. hongmei.ren@wright.edu.ORCID 0000-0003-0210-1502

Funding

Washington University Nutrition Obesity Research CenterP30DK056341 · NIDDK · WASHINGTON UNIVERSITY · PI Dominic N Reeds · 1999 to 2026
$30.2M
The Role of Lipin1 in Myofiber Stability and IntegrityR01AR077574 · NIAMS · WRIGHT STATE UNIVERSITY · PI REN, HONGMEI · 2021 to 2025
$1.8M
LIPIN 1 AND CARDIAC METABOLISM IN THE CONTEXT OF LIPID OVERLOADR01HL119225 · NHLBI · WASHINGTON UNIVERSITY · PI FINCK, BRIAN N · 2014 to 2017
$1.5M
Determining if there is a primary myopathy in Huntington's diseaseR15NS099850 · NINDS · WRIGHT STATE UNIVERSITY · PI VOSS, ANDREW ALVIN · 2018 to 2018
$455k
National Institute of Health 5R01 AR077574National Institute of Health HL119225NHLBI NIH HHS R01 HL119225NIAMS NIH HHS R01 AR077574NIDDK NIH HHS P30 DK056341NINDS NIH HHS NS099850NINDS NIH HHS R15 NS099850U.S. Department of Defense W81XWH2110679
6 · The paper itself

Abstract

backgroundDuchenne muscular dystrophy (DMD) is a progressive and devastating muscle disease, resulting from the absence of dystrophin. This leads to cell membrane instability, susceptibility to contraction-induced muscle damage, subsequent muscle degeneration, and eventually disability and early death of patients. Currently, there is no cure for DMD. Our recent studies identified that lipin1 plays a critical role in maintaining myofiber stability and integrity. However, lipin1 gene expression levels are dramatically reduced in the skeletal muscles of DMD patients and mdx mice.

methodsTo identify whether increased lipin1 expression could prevent dystrophic pathology, we employed unique muscle-specific mdx:lipin1 transgenic (mdx:lipin1

resultsWe found that increased lipin1 expression suppressed muscle degeneration and inflammation, reduced fibrosis, strengthened membrane integrity, and resulted in improved muscle contractile and lengthening force, and muscle performance in mdx:lipin1

conclusionsOverall, our data suggest that lipin1 is a promising therapeutic target for the treatment of dystrophic muscles.

Indexed as

Mice, Inbred mdxMuscle, SkeletalMuscular Dystrophy, DuchennePhosphatidate PhosphataseAnimalsGenetic TherapyMaleMiceMice, Inbred C57BLMice, TransgenicMolecular Targeted TherapyMuscle ContractionLpin1 protein, mousePhosphatidate PhosphataseDMDDystrophinlipin1Membrane integrityMuscular dystrophyPhosphatidic acid phosphataseSkeletal muscleTherapeutic target

Identifiers

PMID39014470
PMCPMC11253568

What OpenQuestion holds

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Registered trials

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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.