Focusing on fibrosis: halofuginone-induced functional improvement in the mdx mouse model of Duchenne muscular dystrophy
Author:
Publisher
American Physiological Society
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology
Link
https://www.physiology.org/doi/pdf/10.1152/ajpheart.00176.2008
Reference46 articles.
1. Implication of the satellite cell in dystrophic muscle fibrosis: a self-perpetuating mechanism of collagen overproduction
2. Immunomodulation of TGF-beta1 in mdx mouse inhibits connective tissue proliferation in diaphragm but increases inflammatory response: Implications for antifibrotic therapy
3. Treatment of the heart in Duchenne muscular dystrophy
4. Functional improvement of dystrophic muscle by myostatin blockade
5. Dystrophin‐deficient mdx mice display a reduced life span and are susceptible to spontaneous rhabdomyosarcoma
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1. Combined gene therapy via VEGF and mini-dystrophin synergistically improves pathologies in temporalis muscle of dystrophin/utrophin double knockout mice;Human Molecular Genetics;2021-05-13
2. Genetic ablation of P65 subunit of NF‐κB in mdx mice to improve muscle physiological function;Muscle & Nerve;2017-05-15
3. Halofuginone attenuates articular cartilage degeneration by inhibition of elevated TGF-β1 signaling in articular cartilage in a rodent osteoarthritis model;Molecular Medicine Reports;2017-05
4. Halofuginone attenuates osteoarthritis by inhibition of TGF-β activity and H-type vessel formation in subchondral bone;Annals of the Rheumatic Diseases;2015-10-15
5. Rapid depletion of muscle progenitor cells in dystrophic mdx/utrophin−/− mice;Human Molecular Genetics;2014-04-29
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