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TNF‐α acts via p38 MAPK to stimulate expression of the ubiquitin ligase atrogin1/MAFbx in skeletal muscle
  • Y. Li, Y. Chen, +4 authors M. Reid
  • Biology, Medicine
  • FASEB journal : official publication of the…
  • 1 March 2005
Atrogin1/MAFbx is an ubiquitin ligase that mediates muscle atrophy in a variety of catabolic states. We recently found that H2O2 stimulates atrogin1/MAFbx gene expression. Since the cytokine tumorExpand
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Oxidative stress, chronic disease, and muscle wasting
Underlying the pathogenesis of chronic disease is the state of oxidative stress. Oxidative stress is an imbalance in oxidant and antioxidant levels. If an overproduction of oxidants overwhelms theExpand
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Bowman-Birk inhibitor concentrate prevents atrophy, weakness, and oxidative stress in soleus muscle of hindlimb-unloaded mice.
Antigravity muscles atrophy and weaken during prolonged mechanical unloading caused by bed rest or spaceflight. Unloading also induces oxidative stress in muscle, a putative cause of weakness. WeExpand
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Doxorubicin acts through tumor necrosis factor receptor subtype 1 to cause dysfunction of murine skeletal muscle.
Cancer patients receiving doxorubicin chemotherapy experience both muscle weakness and fatigue. One postulated mediator of the muscle dysfunction is an increase in tumor necrosis factor-alpha (TNF),Expand
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Doxorubicin acts via mitochondrial ROS to stimulate catabolism in C2C12 myotubes.
Doxorubicin, a commonly prescribed chemotherapeutic agent, causes skeletal muscle wasting in cancer patients undergoing treatment and increases mitochondrial reactive oxygen species (ROS) production.Expand
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Stretch‐stimulated glucose uptake in skeletal muscle is mediated by reactive oxygen species and p38 MAP‐kinase
Alternatives to the canonical insulin‐stimulated pathway for glucose uptake are exercise‐ and exogenous reactive oxygen species (ROS)‐stimulated glucose uptake. We proposed a model wherein mechanicalExpand
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TNF-alpha acts via TNFR1 and muscle-derived oxidants to depress myofibrillar force in murine skeletal muscle.
Tumor necrosis factor-alpha (TNF) diminishes specific force of skeletal muscle. To address the mechanism of this response, we tested the hypothesis that TNF acts via the type 1 (TNFR1) receptorExpand
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TNF induction of atrogin-1/MAFbx mRNA depends on Foxo4 expression but not AKT-Foxo1/3 signaling.
Murine models of starvation-induced muscle atrophy demonstrate that reduced protein kinase B (AKT) function upregulates the atrophy-related gene atrogin-1/MAFbx (atrogin). The mechanism involvesExpand
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Beyond atrophy: redox mechanisms of muscle dysfunction in chronic inflammatory disease
Abstract  Chronic inflammatory diseases such as heart failure, cancer and arthritis have secondary effects on skeletal muscle that cause weakness and exercise intolerance. These symptoms exacerbateExpand
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Interleukin-1 stimulates catabolism in C2C12 myotubes.
Interleukin-1 (IL-1) is an inflammatory cytokine that has been linked to muscle catabolism, a process regulated by muscle-specific E3 proteins of the ubiquitin-proteasome pathway. To address cellularExpand
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