Fibroadipogenic progenitors mediate the ability of HDAC inhibitors to promote regeneration in dystrophic muscles of young, but not old Mdx mice - Wikidata - wikimedia - TriplyDB

Fibroadipogenic progenitors mediate the ability of HDAC inhibitors to promote regeneration in dystrophic muscles of young, but not old Mdx mice

Fibroadipogenic progenitors mediate the ability of HDAC inhibitors to promote regeneration in dystrophic muscles of young, but not old Mdx mice

http://www.wikidata.org/entity/Q36771323

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Molecular and cell-based therapies for muscle degenerations: a road under construction Muscle Satellite Cells: Exploring the Basic Biology to Rule Them Epigenetic Reprogramming of Muscle Progenitors: Inspiration for Clinical Therapies Role of Inflammation in Muscle Homeostasis and Myogenesis Potential of adipose-derived stem cells in muscular regenerative therapies Interactions between muscle stem cells, mesenchymal-derived cells and immune cells in muscle homeostasis, regeneration and disease Chromatin signaling in muscle stem cells: interpreting the regenerative microenvironment Cell death, clearance and immunity in the skeletal muscle Recent advances using zebrafish animal models for muscle disease drug discovery Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trials MicroRNAs modulated by local mIGF-1 expression in mdx dystrophic mice.Muscular dystrophy in the mdx mouse is a severe myopathy compounded by hypotrophy, hypertrophy and hyperplasia.Activation of non-myogenic mesenchymal stem cells during the disease progression in dystrophic dystrophin/utrophin knockout mice.Brahma is required for cell cycle arrest and late muscle gene expression during skeletal myogenesis Characterization of adipocytes derived from fibro/adipogenic progenitors resident in human skeletal muscle Histologic muscular history in steroid-treated and untreated patients with Duchenne dystrophy Muscle-specific microRNAs as biomarkers of Duchenne Muscular Dystrophy progression and response to therapies HDAC-regulated myomiRs control BAF60 variant exchange and direct the functional phenotype of fibro-adipogenic progenitors in dystrophic muscles.Epigenetic control of skeletal muscle regeneration: Integrating genetic determinants and environmental changes Fate choice of post-natal mesoderm progenitors: skeletal versus cardiac muscle plasticity.Role of the TWEAK-Fn14-cIAP1-NF-κB Signaling Axis in the Regulation of Myogenesis and Muscle Homeostasis Skeletal muscle tissue engineering: strategies for volumetric constructs.Invited review: Stem cells and muscle diseases: advances in cell therapy strategies.Histone deacetylase inhibitors: a potential epigenetic treatment for Duchenne muscular dystrophy.Fat deposition and accumulation in the damaged and inflamed skeletal muscle: cellular and molecular players.Drug Discovery of Therapies for Duchenne Muscular Dystrophy.Striated muscle function, regeneration, and repair Could we also be regenerative superheroes, like salamanders?Single Cell Gene Expression Profiling of Skeletal Muscle-Derived Cells.Dystrophic muscle environment induces changes in cell plasticity.Muscle Interstitial Cells: A Brief Field Guide to Non-satellite Cell Populations in Skeletal Muscle.Autophagy regulates satellite cell ability to regenerate normal and dystrophic muscles.Investigating the cellular origin of rotator cuff muscle fatty infiltration and fibrosis after injury.Editorial: Role of Stem Cells in Skeletal Muscle Development, Regeneration, Repair, Aging, and Disease.Pathways Implicated in Tadalafil Amelioration of Duchenne Muscular Dystrophy.Increased levels of interleukin-6 exacerbate the dystrophic phenotype in mdx mice.MiR-23-TrxR1 as a novel molecular axis in skeletal muscle differentiation.The extraocular muscle stem cell niche is resistant to ageing and disease.The HDAC Inhibitor TSA Ameliorates a Zebrafish Model of Duchenne Muscular Dystrophy Adipogenic fate commitment of muscle-derived progenitor cells: isolation, culture, and differentiation.

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Fibroadipogenic progenitors mediate the ability of HDAC inhibitors to promote regeneration in dystrophic muscles of young, but not old Mdx mice

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EMBO Molecular Medicine

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Adamo Diamantini

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Alessandra Sacco

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Chiara Mozzetta

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David Sassoon

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Giovanna Borsellino

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Giovanna Marazzi

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Kathryn J Mitchell

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Luca Battistini

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Matthew Tierney

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Pier Lorenzo Puri

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P2860

Short telomeres and stem cell exhaustion model Duchenne muscular dystrophy in mdx/mTR mice

Sca-1 expression is required for efficient remodeling of the extracellular matrix during skeletal muscle regeneration.

Stage-specific modulation of skeletal myogenesis by inhibitors of nuclear deacetylases.

Defective myoblasts identified in Duchenne muscular dystrophy.

Self-renewal and expansion of single transplanted muscle stem cells.

Muscular dystrophies: genes to pathogenesis.

Muscle stem cells in development, regeneration, and disease.

Intrinsic changes and extrinsic influences of myogenic stem cell function during aging.

HDAC2 blockade by nitric oxide and histone deacetylase inhibitors reveals a common target in Duchenne muscular dystrophy treatment.

The emerging biology of satellite cells and their therapeutic potential.

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626-639

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10.1002/EMMM.201202096

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4

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3628105

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