ArticleCell death & disease2018
Nintedanib decreases muscle fibrosis and improves muscle function in a murine model of dystrophinopathy.
Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 49 citations in OpenAlex.
- Serum biomarkers associated with baseline clinical severity in young steroid-naïve Duchenne muscular dystrophy boys.Human molecular genetics · 2020Trial
- Early effects of antifibrotic therapy on respiratory muscle stiffness and dyspnea in SSc-ILD: a shear wave elastography study.Internal and emergency medicine · 2026Article
- Identification of biomarkers associated with pathological dynamic progression in dystrophinopathies.Scientific reports · 2026Article
- Examining the effectiveness of nintedanib in preventing post-laminectomy epidural fibrosis in rats.Ulusal travma ve acil cerrahi dergisi = Turkish journal of trauma & emergency surgery : TJTES · 2026Article
- Effects of Nintedanib on Orofacial Fibroblasts and Myoblasts.Biomolecules · 2026Article
- Functional Foods, a Hope to Delay Muscle Dystrophy Progression: A Potential Role for Omega Fatty Acids.Nutrients · 2025Review
- Age-related thinning of orbicularis oculi muscle inside upper eyelid and its possible association with sunken upper eyelids.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
- In Sequence Antifibrotic Treatment and Rehabilitation after Volumetric Muscle Loss Injury.Advances in wound care · 2025Article
- Reversing Decline in Aging Muscles: Expected Trends, Impacts and Remedies.Journal of functional morphology and kinesiology · 2025Review
- Strategy for drug repurposing in fibroadipogenic replacement during muscle wasting: application to duchenne muscular dystrophy.Frontiers in cell and developmental biology · 2025Article
- Prospects for the Protective Mechanisms and Compounds of Bufei Huoxue Capsule against COVID-19 Convalescence: Evaluation of Integrating UHPLC-HRMS Analysis and Network Pharmacology Strategy.Combinatorial chemistry & high throughput screening · 2025Article
- l-Carnitine relieves cachexia-related skeletal muscle fibrosis by inducing deltex E3 ubiquitin ligase 3L to negatively regulate the Runx2/COL1A1 axis.Journal of cachexia, sarcopenia and muscle · 2024Article
- MuSCs and IPCs: roles in skeletal muscle homeostasis, aging and injury.Cellular and molecular life sciences : CMLS · 2024Review
- Pharmacotherapeutic Approaches to Treatment of Muscular Dystrophies.Biomolecules · 2023Review
- Spatial transcriptomics reveal markers of histopathological changes in Duchenne muscular dystrophy mouse models.Nature communications · 2023Article
- Molecular and Phenotypic Changes in FLExDUX4 Mice.Journal of personalized medicine · 2023Article
- Exploring skeletal muscle tolerance and whole-body metabolic effects of FDA-approved drugs in a volumetric muscle loss model.Physiological reports · 2023Article
- Article
- Nintedanib Reduces Muscle Fibrosis and Improves Muscle Function of the Alpha-Sarcoglycan-Deficient Mice.Biomedicines · 2022Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Duchenne muscle dystrophy (DMD) is a genetic disorder characterized by progressive skeletal muscle weakness. Dystrophin deficiency induces instability of the sarcolemma during muscle contraction that leads to muscle necrosis and replacement of muscle by fibro-adipose tissue. Several therapies have been developed to counteract the fibrotic process. We report the effects of nintedanib, a tyrosine kinase inhibitor, in the mdx murine model of DMD. Nintedanib reduced proliferation and migration of human fibroblasts in vitro and decreased the expression of fibrotic genes such as COL1A1, COL3A1, FN1, TGFB1, and PDGFA. We treated seven mdx mice with 60 mg/kg/day nintedanib for 1 month. Electrophysiological studies showed an increase in the amplitude of the motor action potentials and an improvement of the morphology of motor unit potentials in the animals treated. Histological studies demonstrated a significant reduction of the fibrotic areas present in the skeletal muscles. Analysis of mRNA expression from muscles of treated mice showed a reduction in Col1a1, Col3a1, Tgfb1, and Pdgfa. Western blot showed a reduction in the expression of collagen I in skeletal muscles. In conclusion, nintedanib reduced the fibrotic process in a murine model of dystrophinopathy after 1 month of treatment, suggesting its potential use as a therapeutic drug in DMD patients.
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