Myonuclear apoptosis in dystrophic mdx muscle occurs by perforin-mediated cytotoxicity.
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Osteopontin promotes fibrosis in dystrophic mouse muscle by modulating immune cell subsets and intramuscular TGF-betaUse of cell permeable NBD peptides for suppression of inflammationMuscular dystrophy begins early in embryonic development deriving from stem cell loss and disrupted skeletal muscle formationMicrotubules underlie dysfunction in duchenne muscular dystrophy.Molecular profiles of Quadriceps muscle in myostatin-null mice reveal PI3K and apoptotic pathways as myostatin targets.A mathematical model of skeletal muscle disease and immune response in the mdx mouse.Regulatory interactions between muscle and the immune system during muscle regenerationGreen tea extract decreases muscle pathology and NF-kappaB immunostaining in regenerating muscle fibers of mdx mice.Matrix metalloproteinase inhibitor batimastat alleviates pathology and improves skeletal muscle function in dystrophin-deficient mdx mice.Equal force recovery in dysferlin-deficient and wild-type muscles following saponin exposure.Stable expression of calpain 3 from a muscle transgene in vivo: immature muscle in transgenic mice suggests a role for calpain 3 in muscle maturation.Alterations in the expression of leukemia inhibitory factor following exercise: comparisons between wild-type and mdx muscles.Interleukin-10 reduces the pathology of mdx muscular dystrophy by deactivating M1 macrophages and modulating macrophage phenotype.Cytoplasmic gamma-actin contributes to a compensatory remodeling response in dystrophin-deficient muscleInterleukin-15 administration improves diaphragm muscle pathology and function in dystrophic mdx mice.Osteopontin-stimulated expression of matrix metalloproteinase-9 causes cardiomyopathy in the mdx model of Duchenne muscular dystrophyUp-regulation of MHC class I expression accompanies but is not required for spontaneous myopathy in dysferlin-deficient SJL/J mice.Eosinophilia of dystrophin-deficient muscle is promoted by perforin-mediated cytotoxicity by T cell effectors.Sulforaphane Attenuates Muscle Inflammation in Dystrophin-deficient mdx Mice via NF-E2-related Factor 2 (Nrf2)-mediated Inhibition of NF-κB Signaling PathwayDystrophin and dysferlin double mutant mice: a novel model for rhabdomyosarcomaalpha-Dystroglycan is a laminin receptor involved in extracellular matrix assembly on myotubes and muscle cell viability.Loss of calpain 3 proteolytic activity leads to muscular dystrophy and to apoptosis-associated IkappaBalpha/nuclear factor kappaB pathway perturbation in mice.A nitric oxide synthase transgene ameliorates muscular dystrophy in mdx miceMuscle-specific expression of insulin-like growth factor I counters muscle decline in mdx mice.The peroxisome proliferator-activated receptor γ coactivator 1α/β (PGC-1) coactivators repress the transcriptional activity of NF-κB in skeletal muscle cellsMajor basic protein-1 promotes fibrosis of dystrophic muscle and attenuates the cellular immune response in muscular dystrophy.Regulatory T cells suppress muscle inflammation and injury in muscular dystrophy.Shifts in macrophage phenotypes and macrophage competition for arginine metabolism affect the severity of muscle pathology in muscular dystrophy.Wasting mechanisms in muscular dystrophy.Partial least squares based identification of Duchenne muscular dystrophy specific genes.Mitochondrial alterations and oxidative stress in an acute transient mouse model of muscle degeneration: implications for muscular dystrophy and related muscle pathologies.Klotho gene silencing promotes pathology in the mdx mouse model of Duchenne muscular dystrophy.Immune-mediated mechanisms potentially regulate the disease time-course of duchenne muscular dystrophy and provide targets for therapeutic intervention.Contribution of oxidative stress to pathology in diaphragm and limb muscles with Duchenne muscular dystrophy.Role of the TWEAK-Fn14-cIAP1-NF-κB Signaling Axis in the Regulation of Myogenesis and Muscle HomeostasisEffects of T-lymphocyte depletion on muscle fibrosis in the mdx mouse.Unveiling transcription factor regulation and differential co-expression genes in Duchenne muscular dystrophy.Chemotaxis and Immunoregulatory Function of Cardiac γδ T Cells in Dystrophin-Deficient Mice.IGF-II ameliorates the dystrophic phenotype and coordinately down-regulates programmed cell death.Bcl-2 overexpression prevents calcium overload and subsequent apoptosis in dystrophic myotubes.
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Myonuclear apoptosis in dystrophic mdx muscle occurs by perforin-mediated cytotoxicity.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on June 1997
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Myonuclear apoptosis in dystrophic mdx muscle occurs by perforin-mediated cytotoxicity.
@en
Myonuclear apoptosis in dystrophic mdx muscle occurs by perforin-mediated cytotoxicity.
@nl
type
label
Myonuclear apoptosis in dystrophic mdx muscle occurs by perforin-mediated cytotoxicity.
@en
Myonuclear apoptosis in dystrophic mdx muscle occurs by perforin-mediated cytotoxicity.
@nl
prefLabel
Myonuclear apoptosis in dystrophic mdx muscle occurs by perforin-mediated cytotoxicity.
@en
Myonuclear apoptosis in dystrophic mdx muscle occurs by perforin-mediated cytotoxicity.
@nl
P2093
P2860
P356
P1476
Myonuclear apoptosis in dystrophic mdx muscle occurs by perforin-mediated cytotoxicity.
@en
P2093
Dorshkind KA
Rodriguez EM
Spencer MJ
Tidball JG
P2860
P304
P356
10.1172/JCI119464
P407
P577
1997-06-01T00:00:00Z