Muscle Satellite Cells and Duchenne Muscular Dystrophy

Miyagoe-Suzuki, Yuko; Fukada, So‐ichiro; Takeda, Shin’ichi

doi:10.5772/30769

Cited by 2 publications

(3 citation statements)

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“…This leads to impaired signal transduction and transcriptional activity in the newly generated cells [227]. The defects in polarization, centrosome amplification, and prolonged cell divisions of dystrophic ASCs have been attributed to the loss of dystrophin interaction with MARK2 [228][229][230][231] as well as downregulation and mislocalization of another DGC component, β-syntrophin. Generally, β-syntrophin interacts with p38γ, modulating CARM1-mediated activation of MYF5 in the opposite cell that undergoes myogenic differentiation [232], while dystrophin deficiency leads to impaired polarization of p38γ, enhanced phosphorylation of CARM1, and reduced ability of MYF5 to be activated by PAX7 [233].…”

Section: Dystrophin Deficiency In Muscle Regenerationmentioning

confidence: 99%

Epigenetic modifications in muscle regeneration and progression of Duchenne muscular dystrophy

2021

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Duchenne muscular dystrophy (DMD) is a multisystemic disorder that affects 1:5000 boys. The severity of the phenotype varies dependent on the mutation site in the DMD gene and the resultant dystrophin expression profile. In skeletal muscle, dystrophin loss is associated with the disintegration of myofibers and their ineffective regeneration due to defective expansion and differentiation of the muscle stem cell pool. Some of these phenotypic alterations stem from the dystrophin absence-mediated serine–threonine protein kinase 2 (MARK2) misplacement/downregulation in activated muscle stem (satellite) cells and neuronal nitric oxide synthase loss in cells committed to myogenesis. Here, we trace changes in DNA methylation, histone modifications, and expression of regulatory noncoding RNAs during muscle regeneration, from the stage of satellite cells to myofibers. Furthermore, we describe the abrogation of these epigenetic regulatory processes due to changes in signal transduction in DMD and point to therapeutic treatments increasing the regenerative potential of diseased muscles based on this acquired knowledge.

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Section: Dystrophin Deficiency In Muscle Regenerationmentioning

confidence: 99%

Epigenetic modifications in muscle regeneration and progression of Duchenne muscular dystrophy

2021

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“…Mesoangioblasts are characterized as CD34 + /c-kit -/Flk1 + /NKX2.5 -/Myf5 -/Oct4 -/AP + /CD44 + /CD140a + /CD140b + and are multipotent stem cells isolated from blood vessels [1,178].…”

Section: Myoblast Derivation From Mesoangioblastsmentioning

confidence: 99%

“…Duchenne muscular dystrophy (DMD) is a progressive disease caused by mutations in the Xlinked dystrophin gene that is characterized by a lack of dystrophin protein and chronic cycles of myofiber degeneration/regeneration, leading to the replacement of muscular tissue with adipose and fibrotic tissue in the advanced stages of the disease [1,2]. This muscular degeneration progressively leads to severe symptoms such as disability and eventually death.…”

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confidence: 99%

Stem Cell Differentiation Toward the Myogenic Lineage for Muscle Tissue Regeneration: A Focus on Muscular Dystrophy

Ostrovidov

Shi

Sadeghian

et al. 2015

Stem Cell Rev and Rep

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Skeletal muscle tissue engineering is one of the important ways for regenerating functionally defective muscles. Among the myopathies, the Duchenne muscular dystrophy (DMD) is a progressive disease due to mutations of the dystrophin gene leading to progressive myofiber degeneration with severe symptoms. Although current therapies in muscular dystrophy are still very challenging, important progress has been made in materials science and in cellular technologies with the use of stem cells. It is therefore useful to review these advances and the results obtained in a clinical point of view. This article focuses on the differentiation of stem cells into myoblasts, and their application in muscular dystrophy. After an overview of the different stem cells that can be induced to differentiate into the myogenic lineage, we introduce scaffolding materials used for muscular tissue engineering. We then described some widely used methods to differentiate different types of stem cell into myoblasts. We highlight recent insights obtained in therapies for muscular dystrophy. Finally, we conclude with a discussion on stem cell technology. We discussed in parallel the benefits brought by the evolution of the materials and by the expansion of cell sources which can differentiate into myoblasts. We also discussed on future challenges for clinical applications and how to accelerate the translation from the research to the clinic in the frame of DMD.

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Muscle Satellite Cells and Duchenne Muscular Dystrophy

Cited by 2 publications

References 100 publications

Epigenetic modifications in muscle regeneration and progression of Duchenne muscular dystrophy

Epigenetic modifications in muscle regeneration and progression of Duchenne muscular dystrophy

Stem Cell Differentiation Toward the Myogenic Lineage for Muscle Tissue Regeneration: A Focus on Muscular Dystrophy

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