Cancer- and endotoxin-induced cachexia require intact glucocorticoid signaling in skeletal muscle. - Wikidata - awgldk - TriplyDB

Cancer- and endotoxin-induced cachexia require intact glucocorticoid signaling in skeletal muscle.

Cancer- and endotoxin-induced cachexia require intact glucocorticoid signaling in skeletal muscle.

http://www.wikidata.org/entity/Q37118756

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The central role of hypothalamic inflammation in the acute illness response and cachexia Reactive Oxygen Species/Nitric Oxide Mediated Inter-Organ Communication in Skeletal Muscle Wasting Diseases.Toll-like receptor 4 mediates Lewis lung carcinoma-induced muscle wasting via coordinate activation of protein degradation pathways Muscle atrophy in response to cytotoxic chemotherapy is dependent on intact glucocorticoid signaling in skeletal muscle.Aerobic exercise training prevents heart failure-induced skeletal muscle atrophy by anti-catabolic, but not anabolic actions.The regulation of muscle mass by endogenous glucocorticoids.THE EFFECT OF GLUCOCORTICOIDS ON BONE AND MUSCLE The calcium-sensing receptor as a mediator of inflammation.Emerging role for regulated in development and DNA damage 1 (REDD1) in the regulation of skeletal muscle metabolism.Hypothalamic activation is essential for endotoxemia-induced acute muscle wasting.Heat Stress Modulates Both Anabolic and Catabolic Signaling Pathways Preventing Dexamethasone-Induced Muscle Atrophy In Vitro Lipopolysaccharide (LPS) and tumor necrosis factor alpha (TNFα) blunt the response of Neuropeptide Y/Agouti-related peptide (NPY/AgRP) glucose inhibited (GI) neurons to decreased glucose.Insulin ameliorating endotoxaemia-induced muscle wasting is associated with the alteration of hypothalamic neuropeptides and inflammation in rats.Nutrient-induced stimulation of protein synthesis in mouse skeletal muscle is limited by the mTORC1 repressor REDD1.Interleukin-1β signaling in fenestrated capillaries is sufficient to trigger sickness responses in mice.Serum and urine metabolomics study reveals a distinct diagnostic model for cancer cachexia.Fenofibrate prevents skeletal muscle loss in mice with lung cancer.Glucocorticoid Signaling in Health and Disease: Insights From Tissue-Specific GR Knockout Mice.Group I Paks support muscle regeneration and counteract cancer-associated muscle atrophy.The Electrical Stimulation of the Bed Nucleus of the Stria Terminalis Causes Oxidative Stress in Skeletal Muscle of Rats.High-intensity eccentric training ameliorates muscle wasting in colon 26 tumor-bearing mice.The AMPK agonist 5-aminoimidazole-4-carboxamide ribonucleotide (AICAR), but not metformin, prevents inflammation-associated cachectic muscle wasting.

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Cancer- and endotoxin-induced cachexia require intact glucocorticoid signaling in skeletal muscle.

http://www.wikidata.org/entity/Q37118756

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 03 June 2013

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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name

Cancer- and endotoxin-induced ...... signaling in skeletal muscle.

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Cancer- and endotoxin-induced ...... signaling in skeletal muscle.

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Cancer- and endotoxin-induced ...... signaling in skeletal muscle.

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Cancer- and endotoxin-induced ...... signaling in skeletal muscle.

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Cancer- and endotoxin-induced ...... signaling in skeletal muscle.

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Cancer- and endotoxin-induced ...... signaling in skeletal muscle.

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Cancer- and endotoxin-induced ...... signaling in skeletal muscle.

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Aaron J Grossberg

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Anthony P Barnes

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Daniel L Marks

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J Gabriel Knoll

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Julia E Maxson

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Marek Szumowski

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Peter R Levasseur

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Stephanie M Krasnow

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Theodore P Braun

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Xin Xia Zhu

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P2860

Atrogin-1, a muscle-specific F-box protein highly expressed during muscle atrophy

Identification of ubiquitin ligases required for skeletal muscle atrophy

FoxO3 controls autophagy in skeletal muscle in vivo

Foxo transcription factors induce the atrophy-related ubiquitin ligase atrogin-1 and cause skeletal muscle atrophy

Cachexia in cancer patients.

Metabolic acidosis stimulates muscle protein degradation by activating the adenosine triphosphate-dependent pathway involving ubiquitin and proteasomes

Crosstalk between glucocorticoid receptor and nutritional sensor mTOR in skeletal muscle.

Toll-like receptor 4 mediates lipopolysaccharide-induced muscle catabolism via coordinate activation of ubiquitin-proteasome and autophagy-lysosome pathways.

Targeted ablation of TRAF6 inhibits skeletal muscle wasting in mice.

Metabolic acidosis stimulates protein degradation in rat muscle by a glucocorticoid-dependent mechanism.

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3572-3582

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scholarly article

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10.1096/FJ.13-230375

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2013-06-03T00:00:00Z

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23733748

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