Arginine metabolism by macrophages promotes cardiac and muscle fibrosis in mdx muscular dystrophy. - Wikidata - awgldk - TriplyDB

Arginine metabolism by macrophages promotes cardiac and muscle fibrosis in mdx muscular dystrophy.

Arginine metabolism by macrophages promotes cardiac and muscle fibrosis in mdx muscular dystrophy.

http://www.wikidata.org/entity/Q33588636

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Extrinsic and intrinsic control of macrophage inflammatory responses Therapeutic strategies for preventing skeletal muscle fibrosis after injury Muscle fatigue, nNOS and muscle fiber atrophy in limb girdle muscular dystrophy Neuronal nitric oxide synthase-rescue of dystrophin/utrophin double knockout mice does not require nNOS localization to the cell membrane Interleukin-10 reduces the pathology of mdx muscular dystrophy by deactivating M1 macrophages and modulating macrophage phenotype.Lengthening-contractions in isolated myocardium impact force development and worsen cardiac contractile function in the mdx mouse model of muscular dystrophy.Arginase inhibition augments nitric oxide production and facilitates left ventricular systolic function in doxorubicin-induced cardiomyopathy in mice.Adoptive transfer of regulatory T cells protects against Coxsackievirus B3-induced cardiac fibrosis.Nitrosative stress elicited by nNOSµ delocalization inhibits muscle force in dystrophin-null mice IFN-γ promotes muscle damage in the mdx mouse model of Duchenne muscular dystrophy by suppressing M2 macrophage activation and inhibiting muscle cell proliferation Increases of M2a macrophages and fibrosis in aging muscle are influenced by bone marrow aging and negatively regulated by muscle-derived nitric oxide.Implicating exudate macrophages and Ly-6C(high) monocytes in CCR2-dependent lung fibrosis following gene-targeted alveolar injury.Microbial metabolite butyrate facilitates M2 macrophage polarization and function.Macrophage phenotypes during tissue repair.Novel compounds for the treatment of Duchenne muscular dystrophy: emerging therapeutic agents Long-term wheel running compromises diaphragm function but improves cardiac and plantarflexor function in the mdx mouse Klotho gene silencing promotes pathology in the mdx mouse model of Duchenne muscular dystrophy.Expression of intercellular adhesion molecule-1 by myofibers in mdx mice Molecular alterations in skeletal muscle in rheumatoid arthritis are related to disease activity, physical inactivity, and disability.Shared signaling systems in myeloid cell-mediated muscle regeneration.Cardiac and respiratory dysfunction in Duchenne muscular dystrophy and the role of second messengers.Mechanisms of muscle injury, repair, and regeneration.Nitric oxide synthase deficiency and the pathophysiology of muscular dystrophy.Regulation of muscle growth and regeneration by the immune system The significance of macrophage polarization subtypes for animal models of tissue fibrosis and human fibrotic diseases Chemotaxis and Immunoregulatory Function of Cardiac γδ T Cells in Dystrophin-Deficient Mice.Macrophage activation and skeletal muscle healing following traumatic injury.Understanding the process of fibrosis in Duchenne muscular dystrophy.Macrophage density in pharyngeal and laryngeal muscles greatly exceeds that in other striated muscles: an immunohistochemical study using elderly human cadavers.Treatment with the anti-IL-6 receptor antibody attenuates muscular dystrophy via promoting skeletal muscle regeneration in dystrophin-/utrophin-deficient mice.Calcitriol enhances fat synthesis factors and calpain activity in co-cultured cells.Novel and optimized strategies for inducing fibrosis in vivo: focus on Duchenne Muscular Dystrophy Shifts in macrophage cytokine production drive muscle fibrosis.Macrophages escape Klotho gene silencing in the mdx mouse model of Duchenne muscular dystrophy and promote muscle growth and increase satellite cell numbers through a Klotho-mediated pathway.Skeletal muscle regeneration is modulated by inflammation.Fibrosis-Inducing Strategies in Regenerating Dystrophic and Normal Skeletal Muscle.Exosome-Mediated Benefits of Cell Therapy in Mouse and Human Models of Duchenne Muscular Dystrophy.

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Arginine metabolism by macrophages promotes cardiac and muscle fibrosis in mdx muscular dystrophy.

http://www.wikidata.org/entity/Q33588636

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2010 nî lūn-bûn

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2010 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2010年の論文

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Arginine metabolism by macroph ...... sis in mdx muscular dystrophy.

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Kenneth P Roos

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Maria C Jordan

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Tomomi Gotoh

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P2860

Nitric oxide synthase complexed with dystrophin and absent from skeletal muscle sarcolemma in Duchenne muscular dystrophy

Osteopontin promotes fibrosis in dystrophic mouse muscle by modulating immune cell subsets and intramuscular TGF-beta

Long-term blinded placebo-controlled study of SNT-MC17/idebenone in the dystrophin deficient mdx mouse: cardiac protection and improved exercise performance

Absence of alpha-syntrophin leads to structurally aberrant neuromuscular synapses deficient in utrophin

Arginase modulates myocardial contractility by a nitric oxide synthase 1-dependent mechanism

The chemokine system in diverse forms of macrophage activation and polarization

Dystrophin: the protein product of the Duchenne muscular dystrophy locus

Echocardiographic evaluation of fibrous replacement in the myocardium of patients with Duchenne muscular dystrophy

Overexpression of catalase targeted to mitochondria attenuates murine cardiac aging.

92-kD gelatinase is produced by eosinophils at the site of blister formation in bullous pemphigoid and cleaves the extracellular domain of recombinant 180-kD bullous pemphigoid autoantigen.

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