ArticleHuman molecular genetics2014
Distinct roles of TRAF6 at early and late stages of muscle pathology in the mdx model of Duchenne muscular dystrophy.
Article in Human molecular genetics, 2014. 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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Who cites it
20 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- The Immune System in Duchenne Muscular Dystrophy Pathogenesis.Biomedicines · 2021Review
- Defective dystrophic thymus determines degenerative changes in skeletal muscle.Nature communications · 2021Article
- Ubiquitin Ligases at the Heart of Skeletal Muscle Atrophy Control.Molecules (Basel, Switzerland) · 2021Review
- The Role of Autophagy in Skeletal Muscle Diseases.Frontiers in physiology · 2021Review
- Matrix Metalloproteinase 13 from Satellite Cells is Required for Efficient Muscle Growth and Regeneration.Cellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2020Article
- PERK regulates skeletal muscle mass and contractile function in adult mice.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- MicroRNA351 targetingJournal of thoracic disease · 2018Article
- Targeting the Muscle-Bone Unit: Filling Two Needs with One Deed in the Treatment of Duchenne Muscular Dystrophy.Current osteoporosis reports · 2018Review
- TAK1 regulates skeletal muscle mass and mitochondrial function.JCI insight · 2018Article
- In Situ Immunofluorescent Staining of Autophagy in Muscle Stem Cells.Journal of visualized experiments : JoVE · 2017Article
- SU9516 Increases α7β1 Integrin and Ameliorates Disease Progression in the mdx Mouse Model of Duchenne Muscular Dystrophy.Molecular therapy : the journal of the American Society of Gene Therapy · 2017Article
- Autophagy regulates satellite cell ability to regenerate normal and dystrophic muscles.Cell death and differentiation · 2016Article
- "Get the Balance Right": Pathological Significance of Autophagy Perturbation in Neuromuscular Disorders.Journal of neuromuscular diseases · 2016Review
- Muscle RANK is a key regulator of Ca2+ storage, SERCA activity, and function of fast-twitch skeletal muscles.American journal of physiology. Cell physiology · 2016Article
- TRAF6 regulates satellite stem cell self-renewal and function during regenerative myogenesis.The Journal of clinical investigation · 2016Article
- P2RX7 purinoceptor: a therapeutic target for ameliorating the symptoms of duchenne muscular dystrophy.PLoS medicine · 2015Article
- D-Amino Acid Substitution of Peptide-Mediated NF-κB Suppression in mdx Mice Preserves Therapeutic Benefit in Skeletal Muscle, but Causes Kidney Toxicity.Molecular medicine (Cambridge, Mass.) · 2015Article
- Muscle LIM protein/CSRP3: a mechanosensor with a role in autophagy.Cell death discovery · 2015Article
- Skeletal muscle homeostasis in duchenne muscular dystrophy: modulating autophagy as a promising therapeutic strategy.Frontiers in aging neuroscience · 2014Review
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Duchenne muscular dystrophy (DMD) is a lethal genetic disorder caused by loss of functional dystrophin protein. Accumulating evidence suggests that the deficiency of dystrophin leads to aberrant activation of many signaling pathways which contribute to disease progression. However, the proximal signaling events leading to the activation of various pathological cascades in dystrophic muscle remain less clear. TNF receptor-associated factor 6 (TRAF6) is an adaptor protein which acts as a signaling intermediate for several receptor-mediated signaling events leading to the context-dependent activation of a number of signaling pathways. TRAF6 is also an E3 ubiquitin ligase and an important regulator of autophagy. However, the role of TRAF6 in pathogenesis of DMD remains unknown. Here, we demonstrate that the levels and activity of TRAF6 are increased in skeletal muscle of mdx (a mouse model of DMD) mice. Targeted deletion of TRAF6 improves muscle strength and reduces fiber necrosis, infiltration of macrophages and the activation of proinflammatory transcription factor nuclear factor-kappa B (NF-κB) in 7-week-old mdx mice. Ablation of TRAF6 also increases satellite cells proliferation and myofiber regeneration in young mdx mice. Intriguingly, ablation of TRAF6 exacerbates muscle injury and increases fibrosis in 9-month-old mdx mice. TRAF6 inhibition reduces the markers of autophagy and Akt signaling in dystrophic muscle of mdx mice. Collectively, our study suggests that while the inhibition of TRAF6 improves muscle structure and function in young mdx mice, its continued inhibition causes more severe myopathy at later stages of disease progression potentially through repressing autophagy.
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