ArticleScience translational medicine2014
Targeting latent TGFβ release in muscular dystrophy.
Article in Science translational medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
What it found
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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.
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Who cites it
40 citing papers in PubMed, 68 citations in OpenAlex.
- The role of mNaunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Combination S100A1 and ARC gene therapy as a treatment for Duchenne muscular dystrophy cardiomyopathy.JCI insight · 2026Article
- LTBP4 deficiency inhibits NLRP3 inflammasome activation in cardiomyocytes and attenuates heart failure in male mice.Nature communications · 2026Article
- The D2.B10-DmdThe American journal of pathology · 2026Article
- Protocol for a Trial to Assess the Efficacy and Applicability of Isometric Strength Training in Older Adults with Sarcopenia and Dynapenia.Healthcare (Basel, Switzerland) · 2025Article
- Collagen type VI regulates TGF-β bioavailability in skeletal muscle in mice.The Journal of clinical investigation · 2025Article
- Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.JCI insight · 2025Article
- Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.bioRxiv : the preprint server for biology · 2025Article
- The extracellular matrix differentially directs myoblast motility and differentiation in distinct forms of muscular dystrophy: Dystrophic matrices alter myoblast motility.Matrix biology : journal of the International Society for Matrix Biology · 2024Article
- The super-healing MRL strain promotes muscle growth in muscular dystrophy through a regenerative extracellular matrix.JCI insight · 2024Article
- The complex landscape of DMD mutations: moving towards personalized medicine.Frontiers in genetics · 2024Review
- Comprehensive analysis of mJournal of translational medicine · 2023Article
- Microdystrophin Gene Addition Significantly Improves Muscle Functionality and Diaphragm Muscle Histopathology in a Fibrotic Mouse Model of Duchenne Muscular Dystrophy.International journal of molecular sciences · 2023Article
- Evaluation of the DBA/2J mouse as a potential background strain for genetic models of cardiomyopathy.Journal of molecular and cellular cardiology plus · 2022Article
- Article
- Targeting the sarcomere in inherited cardiomyopathies.Nature reviews. Cardiology · 2022Review
- Identification of distinct non-myogenic skeletal-muscle-resident mesenchymal cell populations.Cell reports · 2022Article
- Anti-latent TGFβ binding protein 4 antibody improves muscle function and reduces muscle fibrosis in muscular dystrophy.Science translational medicine · 2021Article
- Skeletal Effects of Bone-Targeted TGFbeta Inhibition in a Mouse Model of Duchenne Muscular Dystrophy.Life (Basel, Switzerland) · 2021Article
- Serum Antibodies to N-Glycolylneuraminic Acid Are Elevated in Duchenne Muscular Dystrophy and Correlate with Increased Disease Pathology in CmahThe American journal of pathology · 2021Article
Corrections and comments
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
Latent transforming growth factor-β (TGFβ) binding proteins (LTBPs) bind to inactive TGFβ in the extracellular matrix. In mice, muscular dystrophy symptoms are intensified by a genetic polymorphism that changes the hinge region of LTBP, leading to increased proteolytic susceptibility and TGFβ release. We have found that the hinge region of human LTBP4 was also readily proteolysed and that proteolysis could be blocked by an antibody to the hinge region. Transgenic mice were generated to carry a bacterial artificial chromosome encoding the human LTBP4 gene. These transgenic mice displayed larger myofibers, increased damage after muscle injury, and enhanced TGFβ signaling. In the mdx mouse model of Duchenne muscular dystrophy, the human LTBP4 transgene exacerbated muscular dystrophy symptoms and resulted in weaker muscles with an increased inflammatory infiltrate and greater LTBP4 cleavage in vivo. Blocking LTBP4 cleavage may be a therapeutic strategy to reduce TGFβ release and activity and decrease inflammation and muscle damage in muscular dystrophy.
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Registered trials
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.