ArticleNeuromolecular medicine2012
Differential expression of genes involved in the degeneration and regeneration pathways in mouse models for muscular dystrophies.
Article in Neuromolecular medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 38 citations in OpenAlex.
- Mitochondrial alterations and oxidative stress in an acute transient mouse model of muscle degeneration: implications for muscular dystrophy and related muscle pathologies.The Journal of biological chemistry · 2014Trial
- A novel mouse model foreLife · 2025Article
- Selective ablation of Nfix in macrophages attenuates muscular dystrophy by inhibiting fibro-adipogenic progenitor-dependent fibrosis.The Journal of pathology · 2022Article
- Macrophages in Skeletal Muscle Dystrophies, An Entangled Partner.Journal of neuromuscular diseases · 2022Review
- Shared and distinct mechanisms of skeletal muscle atrophy: A narrative review.Ageing research reviews · 2021Review
- Modeling muscle regeneration in RNA toxicity mice.Human molecular genetics · 2021Article
- (-)-Epicatechin induces mitochondrial biogenesis and markers of muscle regeneration in adults with Becker muscular dystrophy.Muscle & nerve · 2021Article
- Article
- Photobiomodulation therapy protects skeletal muscle and improves muscular function of mdx mice in a dose-dependent manner through modulation of dystrophin.Lasers in medical science · 2018Article
- Genome Editing and Muscle Stem Cells as a Therapeutic Tool for Muscular Dystrophies.Current stem cell reports · 2017Review
- Knockdown of fast skeletal myosin-binding protein C in zebrafish results in a severe skeletal myopathy.The Journal of general physiology · 2016Article
- Muscle Satellite Cells: Exploring the Basic Biology to Rule Them.Stem cells international · 2016Review
- Modifier genes and their effect on Duchenne muscular dystrophy.Current opinion in neurology · 2015Review
- Lack of the serum- and glucocorticoid-inducible kinase SGK1 improves muscle force characteristics and attenuates fibrosis in dystrophic mdx mouse muscle.Pflugers Archiv : European journal of physiology · 2015Article
- ATOH8: a novel marker in human muscle fiber regeneration.Histochemistry and cell biology · 2015Article
- The quasi-parallel lives of satellite cells and atrophying muscle.Frontiers in aging neuroscience · 2015Review
- Wasting mechanisms in muscular dystrophy.The international journal of biochemistry & cell biology · 2013Review
- Coronary adventitial cells are linked to perivascular cardiac fibrosis via TGFβ1 signaling in the mdx mouse model of Duchenne muscular dystrophy.Journal of molecular and cellular cardiology · 2013Article
- Genetic Modifiers for Neuromuscular Diseases.Journal of neuromuscular diseasesArticle
- Effects of endurance exercise and doxorubicin on skeletal muscle myogenic regulatory factor expression.Muscles, ligaments and tendons journalArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The genetically determined muscular dystrophies are caused by mutations in genes coding for muscle proteins. Differences in the phenotypes are mainly the age of onset and velocity of progression. Muscle weakness is the consequence of myofiber degeneration due to an imbalance between successive cycles of degeneration/regeneration. While muscle fibers are lost, a replacement of the degraded muscle fibers by adipose and connective tissues occurs. Major investigation points are to elicit the involved pathophysiological mechanisms to elucidate how each mutation can lead to a specific degenerative process and how the regeneration is stimulated in each case. To answer these questions, we used four mouse models with different mutations causing muscular dystrophies, Dmd (mdx), SJL/J, Large (myd) and Lama2 (dy2J) /J, and compared the histological changes of regeneration and fibrosis to the expression of genes involved in those processes. For regeneration, the MyoD, Myf5 and myogenin genes related to the proliferation and differentiation of satellite cells were studied, while for degeneration, the TGF-β1 and Pro-collagen 1α2 genes, involved in the fibrotic cascade, were analyzed. The result suggests that TGF-β1 gene is activated in the dystrophic process in all the stages of degeneration, while the activation of the expression of the pro-collagen gene possibly occurs in mildest stages of this process. We also observed that each pathophysiological mechanism acted differently in the activation of regeneration, with distinctions in the induction of proliferation of satellite cells, but with no alterations in stimulation to differentiation. Dysfunction of satellite cells can, therefore, be an important additional mechanism of pathogenesis in the dystrophic muscle.
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