ArticleScience translational medicine2021
Anti-latent TGFβ binding protein 4 antibody improves muscle function and reduces muscle fibrosis in muscular dystrophy.
Article in Science translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Genomic and transcriptomic analyses of aortic stenosis enhance therapeutic target discovery and disease prediction.Nature genetics · 2026Pooled it
- LTBP4 deficiency inhibits NLRP3 inflammasome activation in cardiomyocytes and attenuates heart failure in male mice.Nature communications · 2026Article
- RUNX2 Activation in Fibro/Adipogenic Progenitors Promotes Muscle Fibrosis in Muscular Dystrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Muscle-specific increased expression ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Collagen type VI regulates TGF-β bioavailability in skeletal muscle in mice.The Journal of clinical investigation · 2025Article
- Extracellular matrix in skeletal muscle injury and atrophy: mechanisms and therapeutic implications.Journal of orthopaedic translation · 2025Review
- Integrated multi-omics analysis and experimental verification reveal the involvement of the PI3K/Akt signaling pathway in myometrial fibrosis of adenomyosis.Scientific reports · 2025Article
- Repeated birth injuries lead to long-term pelvic floor muscle dysfunction in the preclinical rat model.American journal of obstetrics and gynecology · 2025Article
- miR-27b-3p reduces muscle fibrosis during chronic skeletal muscle injury by targeting TGF-βR1/Smad pathway.Journal of orthopaedic surgery and research · 2024Article
- Matrin3 mediates differentiation through stabilizing chromatin loop-domain interactions and YY1 mediated enhancer-promoter interactions.Nature communications · 2024Article
- Matrisome and Immune Pathways Contribute to Extreme Vascular Outcomes in Williams-Beuren Syndrome.Journal of the American Heart Association · 2024Article
- The super-healing MRL strain promotes muscle growth in muscular dystrophy through a regenerative extracellular matrix.JCI insight · 2024Article
- GDF8 inhibition enhances musculoskeletal recovery and mitigates posttraumatic osteoarthritis following joint injury.Science advances · 2023Article
- Latent transforming growth factor beta binding protein 4: A regulator of mitochondrial function in acute kidney injury.Aging cell · 2023Review
- Pharmacotherapeutic Approaches to Treatment of Muscular Dystrophies.Biomolecules · 2023Review
- Is it time for genetic modifiers to predict prognosis in Duchenne muscular dystrophy?Nature reviews. Neurology · 2023Review
- Modulating fast skeletal muscle contraction protects skeletal muscle in animal models of Duchenne muscular dystrophy.The Journal of clinical investigation · 2023Article
- A FRET-based respirasome assembly screen identifies spleen tyrosine kinase as a target to improve muscle mitochondrial respiration and exercise performance in mice.Nature communications · 2023Article
- Nintedanib Reduces Muscle Fibrosis and Improves Muscle Function of the Alpha-Sarcoglycan-Deficient Mice.Biomedicines · 2022Article
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Authors and funding
16 authors at 2 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy, like other muscular dystrophies, is a progressive disorder hallmarked by muscle degeneration, inflammation, and fibrosis. Latent transforming growth factor β (TGFβ) binding protein 4 (LTBP4) is an extracellular matrix protein found in muscle. LTBP4 sequesters and inhibits a precursor form of TGFβ. LTBP4 was originally identified from a genome-wide search for genetic modifiers of muscular dystrophy in mice, where there are two different alleles. The protective form of LTBP4, which contains an insertion of 12 amino acids in the protein’s hinge region, was linked to increased sequestration of latent TGFβ, enhanced muscle membrane stability, and reduced muscle fibrosis. The deleterious form of LTBP4 protein, lacking 12 amino acids, was more susceptible to proteolysis and promoted release of latent TGF-β, and together, these data underscored the functional role of LTBP4’s hinge. Here, we generated a monoclonal human anti-LTBP4 antibody directed toward LTBP4’s hinge region. In vitro, anti-LTBP4 bound LTBP4 protein and reduced LTBP4 proteolytic cleavage. In isolated myofibers, the LTBP4 antibody stabilized the sarcolemma from injury. In vivo, anti-LTBP4 treatment of dystrophic mice protected muscle against force loss induced by eccentric contraction. Anti-LTBP4 treatment also reduced muscle fibrosis and enhanced muscle force production, including in the diaphragm muscle, where respiratory function was improved. Moreover, the anti-LTBP4 in combination with prednisone, a standard of care for Duchenne muscular dystrophy, further enhanced muscle function and protected against injury in
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