Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1590/0004-282X20170086 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Fibroblast growth factor-inducible 14 regulates satellite cell self-renewal and expansion during skeletal muscle repair.
JCI Insight
January 2025
Institute of Muscle Biology and Cachexia, University of Houston College of Pharmacy, Houston, United States of America.
Skeletal muscle regeneration in adults is predominantly driven by satellite cells. Loss of satellite cell pool and function leads to skeletal muscle wasting in many conditions and disease states. Here, we demonstrate that the levels of fibroblast growth factor-inducible 14 (Fn14) were increased in satellite cells after muscle injury.
View Article and Find Full Text PDFInhibition of hippocampal interleukin-6 receptor-evoked signalling normalises long-term potentiation in dystrophin-deficient mice.
Brain Behav Immun Health
February 2025
Department of Physiology, School of Medicine, University College Cork, Western Road, Cork, Ireland.
Duchenne muscular dystrophy (DMD), an X-linked neuromuscular disorder, characterised by progressive immobility, chronic inflammation and premature death, is caused by the loss of the mechano-transducing signalling molecule, dystrophin. In non-contracting cells, such as neurons, dystrophin is likely to have a functional role in synaptic plasticity, anchoring post-synaptic receptors. Dystrophin-expressing hippocampal neurons are key to cognitive functions such as emotions, learning and the consolidation of memories.
View Article and Find Full Text PDFLabel-free proteomic analysis of Duchenne and Becker muscular dystrophy showed decreased sarcomere proteins and increased ubiquitination-related proteins.
Sci Rep
January 2025
Graduate Course in Medicine (Pathological Anatomy), Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.
Muscular dystrophies (MD) are a group of hereditary diseases marked by progressive muscle loss, leading to weakness and degeneration of skeletal muscles. These conditions often result from structural defects in the Dystrophin-Glycoprotein Complex (DGC), as seen in Duchenne Muscular Dystrophy (DMD) and Becker Muscular Dystrophy (BMD). Since MDs currently have no cure, research has focused on identifying potential therapeutic targets to improve patients' quality of life.
View Article and Find Full Text PDFPharmacological and non-pharmacological therapies for prevention and treatment of osteoporosis in Duchenne Muscular Dystrophy: A systematic review.
Bone
January 2025
Department of Paediatric Endocrinology, Royal Hospital for Children, Glasgow, United Kingdom; School of Medicine, Dentistry & Nursing, University of Glasgow, United Kingdom. Electronic address:
Background: Long term glucocorticoid treatment in Duchenne Muscular Dystrophy (DMD) is associated with a high incidence of fragility fractures. This systematic review aims to assess the current evidence for pharmacological and non-pharmacological treatment for osteoporosis in children and adults with DMD.
Methods: Three online databases (Embase, Medline, Cochrane Library) were searched for studies that evaluated interventions for treatment or prevention of osteoporosis in DMD.
Review of upper extremity passive joint impedance identification in people with Duchenne Muscular Dystrophy.
J Neuroeng Rehabil
January 2025
Department of BioMechanical Engineering, Delft University of Technology, Mekelweg 2, Delft, 2628 CD, South-Holland, The Netherlands.
Duchenne Muscular Dystrophy (DMD) progressively leads to loss of limb function due to muscle weakness. The incurable nature of the disease shifts the focus to improving quality of life, including assistive supports to improve arm function. Over time, the passive joint impedance (Jimp) of people with DMD increases.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!