Lipid peroxidation inhibition blunts nuclear factor-kappaB activation, reduces skeletal muscle degeneration, and enhances muscle function in mdx mice. - Wikidata - awgldk - TriplyDB

Lipid peroxidation inhibition blunts nuclear factor-kappaB activation, reduces skeletal muscle degeneration, and enhances muscle function in mdx mice.

Lipid peroxidation inhibition blunts nuclear factor-kappaB activation, reduces skeletal muscle degeneration, and enhances muscle function in mdx mice.

http://www.wikidata.org/entity/Q35087995

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Investigation of Debio 025, a cyclophilin inhibitor, in the dystrophic mdx mouse, a model for Duchenne muscular dystrophy Inhibitory control over Ca(2+) sparks via mechanosensitive channels is disrupted in dystrophin deficient muscle but restored by mini-dystrophin expression The role of oxidative stress in skeletal muscle injury and regeneration: focus on antioxidant enzymes L-type Ca2+ channel function is linked to dystrophin expression in mammalian muscle Microarchitecture is severely compromised but motor protein function is preserved in dystrophic mdx skeletal muscle.Therapeutic targeting of signaling pathways in muscular dystrophy.RhoA mediates defective stem cell function and heterotopic ossification in dystrophic muscle of mice.Therapeutic potential of proteasome inhibition in Duchenne and Becker muscular dystrophies Skeletal muscle NADPH oxidase is increased and triggers stretch-induced damage in the mdx mouse.Green tea extract decreases muscle pathology and NF-kappaB immunostaining in regenerating muscle fibers of mdx mice.Selective modulation through the glucocorticoid receptor ameliorates muscle pathology in mdx mice Delayed cardiomyopathy in dystrophin deficient mdx mice relies on intrinsic glutathione resource.Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trials Nuclear factor-kappa B signaling in skeletal muscle atrophy.Peptide-based inhibition of NF-κB rescues diaphragm muscle contractile dysfunction in a murine model of Duchenne muscular dystrophy.NBD delivery improves the disease phenotype of the golden retriever model of Duchenne muscular dystrophy.Reactive oxygen species in skeletal muscle signaling.Modulation of p38 mitogen-activated protein kinase cascade and metalloproteinase activity in diaphragm muscle in response to free radical scavenger administration in dystrophin-deficient Mdx mice.Effect of nuclear factor κB inhibition on serotype 9 adeno-associated viral (AAV9) minidystrophin gene transfer to the mdx mouse.D-Amino Acid Substitution of Peptide-Mediated NF-κB Suppression in mdx Mice Preserves Therapeutic Benefit in Skeletal Muscle, but Causes Kidney Toxicity.Effect of the IL-1 Receptor Antagonist Kineret® on Disease Phenotype in mdx Mice.Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.L-arginine decreases inflammation and modulates the nuclear factor-kappaB/matrix metalloproteinase cascade in mdx muscle fibers.Wasting mechanisms in muscular dystrophy.Skeletal muscle diseases, inflammation, and NF-kappaB signaling: insights and opportunities for therapeutic intervention.Role of inflammation and oxidative stress mediators in gliomas.Protein-DNA array-based identification of transcription factor activities differentially regulated in skeletal muscle of normal and dystrophin-deficient mdx mice.Creatine as an antioxidant.Contribution of oxidative stress to pathology in diaphragm and limb muscles with Duchenne muscular dystrophy.Oxidative stress in muscular dystrophy: from generic evidence to specific sources and targets.Flavocoxid, a nutraceutical approach to blunt inflammatory conditions.The Neuro-Immune Pathophysiology of Central and Peripheral Fatigue in Systemic Immune-Inflammatory and Neuro-Immune Diseases.α-Syntrophin stabilizes catalase to reduce endogenous reactive oxygen species levels during myoblast differentiation.Enalapril treatment discloses an early role of angiotensin II in inflammation- and oxidative stress-related muscle damage in dystrophic mdx mice Activation of NF-kappaB pathway in Duchenne muscular dystrophy: relation to age.Control of DNA integrity in skeletal muscle under physiological and pathological conditions.Redox Control of Skeletal Muscle Regeneration.Improvement of endurance of DMD animal model using natural polyphenols.Proteomic analysis of brain protein expression levels in NF-kappabeta p50 -/- homozygous knockout mice Increased catalase expression improves muscle function in mdx mice

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P2860

Lipid peroxidation inhibition blunts nuclear factor-kappaB activation, reduces skeletal muscle degeneration, and enhances muscle function in mdx mice.

http://www.wikidata.org/entity/Q35087995

description

2006 nî lūn-bûn

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Lipid peroxidation inhibition ...... s muscle function in mdx mice.

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Lipid peroxidation inhibition ...... s muscle function in mdx mice.

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Lipid peroxidation inhibition ...... s muscle function in mdx mice.

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Lipid peroxidation inhibition ...... s muscle function in mdx mice.

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Alessandra Bitto

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Domenica Altavilla

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Francesco Squadrito

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Letteria Minutoli

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M'hammed Aguennouz

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Maria C Monici

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Paolo Seminara

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P2860

Tumor necrosis factor-alpha and muscle wasting: a cellular perspective

The I kappa B kinase (IKK) and NF-kappa B: key elements of proinflammatory signalling

Glycoprotein complex anchoring dystrophin to sarcolemma

Primary structure of dystrophin-associated glycoproteins linking dystrophin to the extracellular matrix

Membrane organization of the dystrophin-glycoprotein complex

Early onset of lipofuscin accumulation in dystrophin-deficient skeletal muscles of DMD patients and mdx mice.

The beginning of the end: IkappaB kinase (IKK) and NF-kappaB activation.

Systemic administration of the NF-kappaB inhibitor curcumin stimulates muscle regeneration after traumatic injury.

Human hepatitis C virus NS5A protein alters intracellular calcium levels, induces oxidative stress, and activates STAT-3 and NF-kappa B.

The role of nuclear factor kappa B in the pathogenesis of pulmonary diseases: implications for therapy.

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