GDF11 does not rescue aging-related pathological hypertrophy - Wikidata - wikimedia - TriplyDB

GDF11 does not rescue aging-related pathological hypertrophy

GDF11 does not rescue aging-related pathological hypertrophy

http://www.wikidata.org/entity/Q28267548

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Geroscience approaches to increase healthspan and slow aging The Role of Exercise in Cardiac Aging: From Physiology to Molecular Mechanisms Role of circulating factors in cardiac aging.Structural basis for potency differences between GDF8 and GDF11.Activin A more prominently regulates muscle mass in primates than does GDF8.Biochemistry and Biology of GDF11 and Myostatin: Similarities, Differences, and Questions for Future Investigation Is Growth Differentiation Factor 11 a Realistic Therapeutic for Aging-Dependent Muscle Defects?Supraphysiological levels of GDF11 induce striated muscle atrophy The elusive philosopher's stone in young blood.Circulating Growth Differentiation Factor 11/8 Levels Decline With Age.Aging and Autophagy in the Heart Serum Levels of Growth Differentiation Factor 11 Are Independently Associated with Low Hemoglobin Values in Hemodialysis Patients Quantification of GDF11 and Myostatin in Human Aging and Cardiovascular Disease.GDF11/BMP11 activates both smad1/5/8 and smad2/3 signals but shows no significant effect on proliferation and migration of human umbilical vein endothelial cells.Molecular circuitry of stem cell fate in skeletal muscle regeneration, ageing and disease.GDF11 decreases bone mass by stimulating osteoclastogenesis and inhibiting osteoblast differentiation.GDF11 improves tubular regeneration after acute kidney injury in elderly mice.GDF11 administration does not extend lifespan in a mouse model of premature aging.Systemic Problems: A perspective on stem cell aging and rejuvenation.Quantitation of circulating GDF-11 and β2-MG in aged patients with age-related impairment in cognitive function.Exogenous GDF11 induces cardiac and skeletal muscle dysfunction and wasting.BMP signalling in skeletal development, disease and repair.Geroprotectors: A Unified Concept and Screening Approaches.Renal Aging: Causes and Consequences.Pathways for salvage and protection of the heart under stress: novel routes for cardiac rejuvenation.Neural Stem Cell Plasticity: Advantages in Therapy for the Injured Central Nervous System Differential Binding Activity of TGF-β Family Proteins to Select TGF-β Receptors.GDF11 Protects against Endothelial Injury and Reduces Atherosclerotic Lesion Formation in Apolipoprotein E-Null Mice.Application of bio-orthogonal proteome labeling to cell transplantation and heterochronic parabiosis.Modulation of GDF11 expression and synaptic plasticity by age and training.Questions and Answers About Myostatin, GDF11, and the Aging Heart.Getting Old through the Blood: Circulating Molecules in Aging and Senescence of Cardiovascular Regenerative Cells.Role of growth differentiation factor 11 in development, physiology and disease.GDF11 Inhibits Bone Formation by Activating Smad2/3 in Bone Marrow Mesenchymal Stem Cells.The pathway to muscle fibrosis depends on myostatin stimulating the differentiation of fibro/adipogenic progenitor cells in chronic kidney disease.Targeted myocardial delivery of GDF11 gene rejuvenates the aged mouse heart and enhances myocardial regeneration after ischemia-reperfusion injury.Young Blood Rejuvenates Old Bodies: A Call for Reflection when Moving from Mice to Men.Muscle Stem Cells: A Model System for Adult Stem Cell Biology.GDF11/BMP11 as a novel tumor marker for liver cancer.Development of an ultra-sensitive Simoa assay to enable GDF11 detection: a comparison across bioanalytical platforms.

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P2860

GDF11 does not rescue aging-related pathological hypertrophy

http://www.wikidata.org/entity/Q28267548

description

2015 nî lūn-bûn

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2015 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

@hyw

2015 թվականի նոյեմբերին հրատարակված գիտական հոդված

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2015年の論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年論文

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2015年论文

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name

GDF11 does not rescue aging-related pathological hypertrophy

@ast

GDF11 does not rescue aging-related pathological hypertrophy

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GDF11 does not rescue aging-related pathological hypertrophy

@nl

type

label

GDF11 does not rescue aging-related pathological hypertrophy

@ast

GDF11 does not rescue aging-related pathological hypertrophy

@en

GDF11 does not rescue aging-related pathological hypertrophy

@nl

prefLabel

GDF11 does not rescue aging-related pathological hypertrophy

@ast

GDF11 does not rescue aging-related pathological hypertrophy

@en

GDF11 does not rescue aging-related pathological hypertrophy

@nl

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CIRCRESAHA.115.307527

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Circulation Research

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GDF11 does not rescue aging-related pathological hypertrophy

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Abdelkarim Sabri

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Ashraf Khalil

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David Hayes

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James Tanner

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Julius Kahn

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Polina Gross

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Priyanka Gupta

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Sadia Mohsin

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Scott MacDonnell

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P2860

A mutation in the myostatin gene increases muscle mass and enhances racing performance in heterozygote dogs

Genetic deletion of myostatin from the heart prevents skeletal muscle atrophy in heart failure

Regulation of skeletal muscle mass in mice by a new TGF-beta superfamily member

Restoring systemic GDF11 levels reverses age-related dysfunction in mouse skeletal muscle

Vascular and neurogenic rejuvenation of the aging mouse brain by young systemic factors

GDF11 Increases with Age and Inhibits Skeletal Muscle Regeneration

Growth differentiation factor 11 is a circulating factor that reverses age-related cardiac hypertrophy

Rejuvenation of aged progenitor cells by exposure to a young systemic environment

The old-age heart: normal aging changes which can produce or mimic cardiac disease.

Mouse strain determines cardiac growth potential.

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926-32

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1117140

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11

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Maria Myzithras

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2015-11-06T00:00:00Z

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26383970

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4636963

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