Obesity increases vascular senescence and susceptibility to ischemic injury through chronic activation of Akt and mTOR. - Wikidata - wikimedia - TriplyDB

Obesity increases vascular senescence and susceptibility to ischemic injury through chronic activation of Akt and mTOR.

Obesity increases vascular senescence and susceptibility to ischemic injury through chronic activation of Akt and mTOR.

http://www.wikidata.org/entity/Q42091923

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Rule-based cell systems model of aging using feedback loop motifs mediated by stress responses Adipose tissue endothelial cells from obese human subjects: differences among depots in angiogenic, metabolic, and inflammatory gene expression and cellular senescence NO signaling and S-nitrosylation regulate PTEN inhibition in neurodegeneration Obesity altered T cell metabolism and the response to infection.Chronic high fat diet induces cardiac hypertrophy and fibrosis in mice.A mouse model of diet-induced obesity and insulin resistance Chronic rapamycin restores brain vascular integrity and function through NO synthase activation and improves memory in symptomatic mice modeling Alzheimer's disease.Mammalian target of rapamycin (mTOR) inhibitors: potential uses and a review of haematological adverse effects.Endothelial PGC-1α mediates vascular dysfunction in diabetes.Rictor is an independent prognostic factor for endometrial carcinoma.Altered nutrient response of mTORC1 as a result of changes in REDD1 expression: effect of obesity vs. REDD1 deficiency.Fat tissue, aging, and cellular senescence.Fasting mitigates immediate hypersensitivity: a pivotal role of endogenous D-beta-hydroxybutyrate.Accelerated and exacerbated effects of high dietary fat on neuronal damage induced by transient cerebral ischemia in the gerbil septum.p16INK4a reporter mice reveal age-promoting effects of environmental toxicants Obesity and diabetes cause cognitive dysfunction in the absence of accelerated β-amyloid deposition in a novel murine model of mixed or vascular dementia.De novo lipogenesis maintains vascular homeostasis through endothelial nitric-oxide synthase (eNOS) palmitoylation.Insulin resistance impairs circulating angiogenic progenitor cell function and delays endothelial regeneration PKD1 mediates negative feedback of PI3K/Akt activation in response to G protein-coupled receptors.Resveratrol modifies risk factors for coronary artery disease in swine with metabolic syndrome and myocardial ischemia The synaptoneurosome transcriptome: a model for profiling the emolecular effects of alcohol Interleukin-7 inhibits tumor-induced CD27-CD28- suppressor T cells: implications for cancer immunotherapy.Role of p38 mitogen-activated protein kinase in vascular endothelial aging: interaction with Arginase-II and S6K1 signaling pathway Single rapamycin administration induces prolonged downward shift in defended body weight in rats The most important tasks for peer reviewers evaluating a randomized controlled trial are not congruent with the tasks most often requested by journal editors.NCI's provocative questions on cancer: some answers to ignite discussion.Cell cycle arrest is not yet senescence, which is not just cell cycle arrest: terminology for TOR-driven aging.Differential Telomere Shortening in Blood versus Arteries in an Animal Model of Type 2 Diabetes.Mechanisms involved in the aging-induced vascular dysfunction.Comparison of rapamycin schedules in mice on high-fat diet.The Akt1-eNOS axis illustrates the specificity of kinase-substrate relationships in vivo.Method parameters' impact on mortality and variability in mouse stroke experiments: a meta-analysis.Aging exacerbates obesity-induced oxidative stress and inflammation in perivascular adipose tissue in mice: a paracrine mechanism contributing to vascular redox dysregulation and inflammation.Cognitive rehabilitation reduces cognitive impairment and normalizes hippocampal CA1 architecture in a rat model of vascular dementia.Common drugs and treatments for cancer and age-related diseases: revitalizing answers to NCI's provocative questions.Exercise Prevents Diet-Induced Cellular Senescence in Adipose Tissue.MTOR-driven quasi-programmed aging as a disposable soma theory: blind watchmaker vs. intelligent designer.Rapamycin extends life- and health span because it slows aging.Mammalian target of rapamycin signaling in cardiac physiology and disease.mTOR signalling: the molecular interface connecting metabolic stress, aging and cardiovascular diseases.

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P2860

Obesity increases vascular senescence and susceptibility to ischemic injury through chronic activation of Akt and mTOR.

http://www.wikidata.org/entity/Q42091923

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2009 nî lūn-bûn

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2009年の論文

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name

Obesity increases vascular sen ...... ic activation of Akt and mTOR.

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Obesity increases vascular sen ...... ic activation of Akt and mTOR.

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Obesity increases vascular sen ...... ic activation of Akt and mTOR.

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Obesity increases vascular sen ...... ic activation of Akt and mTOR.

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Obesity increases vascular sen ...... ic activation of Akt and mTOR.

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Obesity increases vascular sen ...... ic activation of Akt and mTOR.

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Obesity increases vascular sen ...... ic activation of Akt and mTOR.

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Hyung-Hwan Kim

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James K Liao

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Laura E Benjamin

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Michael A Moskowitz

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Naoki Sawada

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Yukio Hiroi

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P2860

Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor

Regulation of endothelium-derived nitric oxide production by the protein kinase Akt

Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation

PRAK is essential for ras-induced senescence and tumor suppression

Phosphorylation and regulation of Akt/PKB by the rictor-mTOR complex

Akt1 regulates pathological angiogenesis, vascular maturation and permeability in vivo

Regulation of longevity and stress resistance by Sch9 in yeast.

TOR, a central controller of cell growth.

Interaction of RAFT1 with gephyrin required for rapamycin-sensitive signaling

Hypothalamic mTOR signaling regulates food intake

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