Dietary copper supplementation reverses hypertrophic cardiomyopathy induced by chronic pressure overload in mice. - Wikidata - wikimedia - TriplyDB

Dietary copper supplementation reverses hypertrophic cardiomyopathy induced by chronic pressure overload in mice.

Dietary copper supplementation reverses hypertrophic cardiomyopathy induced by chronic pressure overload in mice.

http://www.wikidata.org/entity/Q36267201

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CB1 cannabinoid receptors promote oxidative stress and cell death in murine models of doxorubicin-induced cardiomyopathy and in human cardiomyocytes Charting the travels of copper in eukaryotes from yeast to mammals Homocysteine induces cardiac hypertrophy by up-regulating ATP7a expression Copper-induced regression of cardiomyocyte hypertrophy is associated with enhanced vascular endothelial growth factor receptor-1 signalling pathway Copper Transport Protein Antioxidant-1 Promotes Inflammatory Neovascularization via Chaperone and Transcription Factor Function.Impaired Ca(2+)-handling in HIF-1alpha(+/-) mice as a consequence of pressure overload.Cardiac-specific overexpression of HIF-1{alpha} prevents deterioration of glycolytic pathway and cardiac remodeling in streptozotocin-induced diabetic mice.Hypoxia inducible factor-1 improves the negative functional effects of natriuretic peptide and nitric oxide signaling in hypertrophic cardiac myocytes Cardiac copper deficiency activates a systemic signaling mechanism that communicates with the copper acquisition and storage organs.Tetrathiomolybdate protects against bile duct ligation-induced cholestatic liver injury and fibrosis Copper deficiency leads to anemia, duodenal hypoxia, upregulation of HIF-2α and altered expression of iron absorption genes in mice.Hydrogen sulfide mitigates transition from compensatory hypertrophy to heart failure Homocysteine restricts copper availability leading to suppression of cytochrome C oxidase activity in phenylephrine-treated cardiomyocytes.CTR1 silencing inhibits angiogenesis by limiting copper entry into endothelial cells.Rejuvenation: an integrated approach to regenerative medicine.Regression of copper-deficient heart hypertrophy: reduction in the size of hypertrophic cardiomyocytes.Regression of pathological cardiac hypertrophy: signaling pathways and therapeutic targets.Heavy metal ions in normal physiology, toxic stress, and cytoprotection.Reversal of physiological deficits caused by diminished levels of peptidylglycine alpha-amidating monooxygenase by dietary copper Thyroid hormone receptor-beta is associated with coronary angiogenesis during pathological cardiac hypertrophy.Role of copper and homocysteine in pressure overload heart failure Featured Article: Effect of copper on nuclear translocation of copper chaperone for superoxide dismutase-1.Endothelial Antioxidant-1: a Key Mediator of Copper-dependent Wound Healing in vivo.Protection of the heart by treatment with a divalent-copper-selective chelator reveals a novel mechanism underlying cardiomyopathy in diabetic rats.Interactions of peptide amidation and copper: novel biomarkers and mechanisms of neural dysfunction.Supplementing exposure to hypoxia with a copper depleted diet does not exacerbate right ventricular remodeling in mice.Ischemia-induced copper loss and suppression of angiogenesis in the pathogenesis of myocardial infarction.Cellular Interplay between Cardiomyocytes and Nonmyocytes in Cardiac Remodeling.VEGFB-VEGFR1 ameliorates Ang II-induced cardiomyocyte hypertrophy through Ca(2+) -mediated PKG I pathway.Perspectives on the Role and Relevance of Copper in Cardiac Disease.Copper stimulates growth of human umbilical vein endothelial cells in a vascular endothelial growth factor-independent pathway.Copper regulation of hypoxia-inducible factor-1 activity.The association of depressed angiogenic factors with reduced capillary density in the Rhesus monkey model of myocardial ischemia.Copper reverses cardiomyocyte hypertrophy through vascular endothelial growth factor-mediated reduction in the cell size The involvement of vimentin in copper-induced regression of cardiomyocyte hypertrophy.Vascular endothelial growth factor recovers suppressed cytochrome c oxidase activity by restoring copper availability in hypertrophic cardiomyocytes.Brief Communication: Copper suppression of vascular endothelial growth factor receptor-2 is involved in the regression of cardiomyocyte hypertrophy.Copper-induced reduction in myocardial fibrosis is associated with increased matrix metalloproteins in a rat model of cardiac hypertrophy.The Association Between Myocardial Fibrosis and Depressed Capillary Density in Rat Model of Left Ventricular Hypertrophy.Inhibition of osteogenic differentiation of mesenchymal stem cells by copper supplementation.

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Dietary copper supplementation reverses hypertrophic cardiomyopathy induced by chronic pressure overload in mice.

http://www.wikidata.org/entity/Q36267201

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Dietary copper supplementation ...... nic pressure overload in mice.

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Dietary copper supplementation ...... nic pressure overload in mice.

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Dietary copper supplementation ...... nic pressure overload in mice.

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Chang Xiao

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Corey Reynolds

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Jack T Saari

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John W Eaton

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Suresh C Tyagi

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Walter Rodriguez

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Wenke Feng

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Y James Kang

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Youchun Jiang

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Zhanxiang Zhou

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P2860

Fatal infantile cardioencephalomyopathy with COX deficiency and mutations in SCO2, a COX assembly gene

The copper chaperone for superoxide dismutase

Dietary reference intakes: vitamin A, vitamin K, arsenic, boron, chromium, copper, iodine, iron, manganese, molybdenum, nickel, silicon, vanadium, and zinc

Overexpression of metallothionein in the heart of transgenic mice suppresses doxorubicin cardiotoxicity

Copper chelation represses the vascular response to injury

Undetectable intracellular free copper: the requirement of a copper chaperone for superoxide dismutase

Metallothionein transfers zinc to mitochondrial aconitase through a direct interaction in mouse hearts.

A longitudinal investigation of aggregate oral intake of copper.

Vascular endothelial growth factor blockade promotes the transition from compensatory cardiac hypertrophy to failure in response to pressure overload

Trace elements in human physiology and pathology. Copper.

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