Evidence map›Paper›PMID 40050938›Full record

ArticleSkeletal muscle2025

Dysregulated ATX-LPA and YAP/TAZ signaling in dystrophic Sgcd

Cristian Gutiérrez-Rojas, Adriana Córdova-Casanova, Jennifer Faundez-Contreras, Meilyn Cruz-Soca, Felipe S Gallardo, Alexia Bock-Pereda, Juan Carlos Casar, Elisabeth R Barton, Enrique Brandan

Abstract read
In one paragraph

Article in Skeletal muscle, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
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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

9 authors.

Cristian Gutiérrez-RojasEscuela de Kinesiología, Facultad de Ciencias, Pontificia Universidad Católica de Valparaíso, 2340025, Valparaíso, Chile. cristian.gutierrez@pucv.cl.
Adriana Córdova-CasanovaCentro Científico y Tecnológico de Excelencia, Ciencia & Vida, 8580702, Santiago, Chile.
Jennifer Faundez-ContrerasCentro Científico y Tecnológico de Excelencia, Ciencia & Vida, 8580702, Santiago, Chile.
Meilyn Cruz-SocaCentro Científico y Tecnológico de Excelencia, Ciencia & Vida, 8580702, Santiago, Chile.
Felipe S GallardoCentro Científico y Tecnológico de Excelencia, Ciencia & Vida, 8580702, Santiago, Chile.
Alexia Bock-PeredaCentro Científico y Tecnológico de Excelencia, Ciencia & Vida, 8580702, Santiago, Chile.
Juan Carlos CasarDepartamento de Neurología, Pontificia Universidad Católica de Chile, 7820436, Santiago, Chile.
Elisabeth R BartonApplied Physiology and Kinesiology, College of Health and Human Performance, University of Florida, Gainesville, FL, USA.
Enrique BrandanCentro Científico y Tecnológico de Excelencia, Ciencia & Vida, 8580702, Santiago, Chile. enrique.brandan@uss.cl.

Funding

Understanding and Improving Therapies for the Muscular Dystrophies through Noninvasive BiomarkersP50AR052646 · NIAMS · UNIVERSITY OF FLORIDA · PI SWEENEY, H LEE · 2021 to 2024
$6.2M
NIAMS NIH HHS P50 AR052646
6 · The paper itself

Abstract

backgroundSarcoglycanopathies are muscle dystrophies caused by mutations in the genes encoding sarcoglycans (α, β, γ, and δ) that can destabilize the dystrophin-associated glycoprotein complex at the sarcolemma, leaving muscle fibers vulnerable to damage after contraction, followed by inflammatory and fibrotic responses and resulting in muscle weakness and atrophy. Two signaling pathways have been implicated in fibrosis and inflammation in various tissues: autotaxin/lysophosphatidic acid (ATX-LPA) and yes-associated protein 1/transcriptional co-activator with PDZ-binding motif (YAP/TAZ). LPA, synthesized by ATX, can act as a pleiotropic molecule due to its multiple receptors. Two Hippo pathway effectors, YAP/TAZ, can be dephosphorylated by LPA and translocated to the nucleus. They induce several target genes, such as CCN2/CTGF, involved in fibrosis and inflammation. However, no detailed characterization of these processes or whether these pathways change early in the development of sarcoglycanopathy has been evaluated in skeletal muscle.

methodsUsing the δ-sarcoglycan knockout mouse model (Sgcd

resultsWe found that Sgcd

conclusionsThe ATX-LPA axis and the YAP/TAZ signaling pathway, which are involved in inflammation and fibrosis, are dysregulated in skeletal muscle from an early age in Sgcd

Indexed as

Adaptor Proteins, Signal TransducingMuscle, SkeletalMuscular Dystrophy, AnimalSarcoglycansAnimalsCell Cycle ProteinsDisease Models, AnimalFibrosisInflammationLysophospholipase DLysophospholipidsMiceMice, KnockoutPhosphoric Diester HydrolasesPyrophosphatasesSignal TransductionAdaptor Proteins, Signal TransducingCell Cycle Proteinslysophosphatidic acidLysophospholipase DLysophospholipidsPhosphoric Diester HydrolasesPyrophosphatasesSarcoglycansTrans-ActivatorsTranscriptional Coactivator with PDZ-Binding Motif ProteinsTranscription FactorsWwtr1 protein, mouseYap1 protein, mouseYAP-Signaling ProteinsAutotaxinFibrosisInflammationLysophosphatidic acidMuscle mechanicsMuscle regenerationYAP/TAZδ Sarcoglycanopathy

Identifiers

PMID40050938
PMCPMC11884125

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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.