Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice. - Wikidata - awgldk - TriplyDB

Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice.

Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice.

http://www.wikidata.org/entity/Q39798655

about

Effects of fatty acid treatments on the dexamethasone-induced intramuscular lipid accumulation in chickens 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.Wasting in chronic kidney disease PTEN inhibition improves muscle regeneration in mice fed a high-fat diet.Dexamethasone-induced autophagy mediates muscle atrophy through mitochondrial clearance.FOXO3a mediates signaling crosstalk that coordinates ubiquitin and atrogin-1/MAFbx expression during glucocorticoid-induced skeletal muscle atrophy Atrogin-1 affects muscle protein synthesis and degradation when energy metabolism is impaired by the antidiabetes drug berberine.Glucocorticoids increase adipocytes in muscle by affecting IL-4 regulated FAP activity.Corticosteroids and muscle wasting: role of transcription factors, nuclear cofactors, and hyperacetylation Muscle atrophy in chronic kidney disease results from abnormalities in insulin signaling.Skeletal muscle atrophy and the E3 ubiquitin ligases MuRF1 and MAFbx/atrogin-1 αMSH blunts endotoxin-induced MuRF1 and atrogin-1 upregulation in skeletal muscle by modulating NF-κB and Akt/FoxO1 pathway Consequences and therapy of the metabolic acidosis of chronic kidney disease.Myostatin suppression of Akirin1 mediates glucocorticoid-induced satellite cell dysfunction.Mechanisms of muscle wasting in chronic kidney disease Pharmacological inhibition of myostatin suppresses systemic inflammation and muscle atrophy in mice with chronic kidney disease.The regulation of muscle mass by endogenous glucocorticoids.Serum- and glucocorticoid-induced kinase 3 in recycling endosomes mediates acute activation of Na+/H+ exchanger NHE3 by glucocorticoids.Cardiac proteasome activity in muscle ring finger-1 null mice at rest and following synthetic glucocorticoid treatment.Central nervous system inflammation induces muscle atrophy via activation of the hypothalamic-pituitary-adrenal axis.Targeting the myostatin signaling pathway to treat muscle wasting diseases Angiotensin II reduces food intake by altering orexigenic neuropeptide expression in the mouse hypothalamus.Glucocorticoid-induced osteoporosis - a disorder of mesenchymal stromal cells?A cell-autonomous role for the glucocorticoid receptor in skeletal muscle atrophy induced by systemic glucocorticoid exposure.Glucocorticoids Alter CRTC-CREB Signaling in Muscle Cells: Impact on PGC-1α Expression and Atrophy Markers Transcription factor FoxO1, the dominant mediator of muscle wasting in chronic kidney disease, is inhibited by microRNA-486.Genome-wide analysis of glucocorticoid receptor-binding sites in myotubes identifies gene networks modulating insulin signaling.Molecular regulation of urea cycle function by the liver glucocorticoid receptor THE EFFECT OF GLUCOCORTICOIDS ON BONE AND MUSCLE Psychological stress and aging: role of glucocorticoids (GCs)Dose and latency effects of leucine supplementation in modulating glucose homeostasis: opposite effects in healthy and glucocorticoid-induced insulin-resistance states.Overexpression of Glucocorticoid Receptor β Enhances Myogenesis and Reduces Catabolic Gene Expression Identification of neutrophil-derived proteases and angiotensin II as biomarkers of cancer cachexia High Dose Omega-3 Fatty Acid Administration and Skeletal Muscle Protein Turnover in Maintenance Hemodialysis Patients.Cancer- and endotoxin-induced cachexia require intact glucocorticoid signaling in skeletal muscle.Regulation of muscle protein synthesis and the effects of catabolic states.Molecular mechanisms and signaling pathways of angiotensin II-induced muscle wasting: potential therapeutic targets for cardiac cachexia miR-628 Promotes Burn-Induced Skeletal Muscle Atrophy via Targeting IRS1.Effects of insulin resistance on skeletal muscle growth and exercise capacity in type 2 diabetic mouse models.

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P2860

Endogenous glucocorticoids and impaired insulin signaling are both required to stimulate muscle wasting under pathophysiological conditions in mice.

http://www.wikidata.org/entity/Q39798655

description

2009 nî lūn-bûn

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name

Endogenous glucocorticoids and ...... siological conditions in mice.

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Endogenous glucocorticoids and ...... siological conditions in mice.

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Endogenous glucocorticoids and ...... siological conditions in mice.

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Endogenous glucocorticoids and ...... siological conditions in mice.

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Endogenous glucocorticoids and ...... siological conditions in mice.

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Endogenous glucocorticoids and ...... siological conditions in mice.

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Journal of Clinical Investigation

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Endogenous glucocorticoids and ...... siological conditions in mice.

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P2093

Huiling Wang

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In Hee Lee

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Jie Du

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William E Mitch

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Zhaoyong Hu

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P2860

The p85 regulatory subunit of phosphoinositide 3-kinase down-regulates IRS-1 signaling via the formation of a sequestration complex

Akt/mTOR pathway is a crucial regulator of skeletal muscle hypertrophy and can prevent muscle atrophy in vivo

Signalling pathways that mediate skeletal muscle hypertrophy and atrophy

Protein degradation by the ubiquitin-proteasome pathway in normal and disease states

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

Interaction of oestrogen receptor with the regulatory subunit of phosphatidylinositol-3-OH kinase

Glucocorticoid-mediated repression of nuclear factor-kappaB-dependent transcription involves direct interference with transactivation

Modulation of insulin receptor, insulin receptor substrate-1, and phosphatidylinositol 3-kinase in liver and muscle of dexamethasone-treated rats.

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

Molecular balance between the regulatory and catalytic subunits of phosphoinositide 3-kinase regulates cell signaling and survival.

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pathophysiology

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2752071

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