MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart. - Wikidata - awgldk - TriplyDB

MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart.

MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart.

http://www.wikidata.org/entity/Q36795205

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Impact of miRNAs on cardiovascular aging Noncoding RNA control of cellular senescence Age-associated pro-inflammatory remodeling and functional phenotype in the heart and large arteries Heart failure with preserved ejection fraction: molecular pathways of the aging myocardium miR-22 in cardiac remodeling and disease Common variation neighbouring micro-RNA 22 is associated with increased left ventricular mass Integromics network meta-analysis on cardiac aging offers robust multi-layer modular signatures and reveals micronome synergism.Age-Associated Differences in MiRNA Signatures Are Restricted to CD45RO Negative T Cells and Are Associated with Changes in the Cellular Composition, Activation and Cellular Ageing MicroRNAs in age-related diseases.miRNAGE-34 induces cardiac damAGE.Aberrant Expression of Breast Development-Related MicroRNAs, miR-22, miR-132, and miR-212, in Breast Tumor Tissues Aging and the cardiac collagen matrix: Novel mediators of fibrotic remodelling MicroRNAs and lncRNAs in senescence: A re-view.Age-associated downregulation of vasohibin-1 in vascular endothelial cells Crucial Role of miR-433 in Regulating Cardiac Fibrosis Noncoding RNAs and myocardial fibrosis.Non-coding RNAs as direct and indirect modulators of epigenetic mechanism regulation of cardiac fibrosis.Atrial remodeling, fibrosis, and atrial fibrillation.Intracellular signaling of cardiac fibroblasts.MicroRNAs in cardiovascular ageing.Cardiac Physiology of Aging: Extracellular Considerations.The Aging Heart Noncoding RNA as regulators of cardiac fibrosis: current insight and the road ahead.Pathways for salvage and protection of the heart under stress: novel routes for cardiac rejuvenation.Aging: Treating the Older Patient.Cardiac fibrosis in the ageing heart: contributors and mechanisms.microRNA in Cardiovascular Aging and Age-Related Cardiovascular Diseases.MicroRNAs in a hypertrophic heart: from foetal life to adulthood.Desregulated microRNAs in aging-related heart failure.DGCR8 is essential for tumor progression following PTEN loss in the prostate.How to be young at heart? miR-22 as a potential therapeutic target to boost autophagy and protect the old myocardium.The GBAP1 pseudogene acts as a ceRNA for the glucocerebrosidase gene GBA by sponging miR-22-3p Measurement of novel biomarkers to predict chronic heart failure outcomes and left ventricular remodeling.Osteoglycin inhibition by microRNA miR-155 impairs myogenesis.miRNA-22 is a Novel Mediator of Vascular Smooth Muscle Cell Phenotypic Modulation and Neointima Formation.Dysregulation of both miR-140-3p and miR-140-5p in synovial fluid correlate with osteoarthritis severity.Advanced glycation end-products accelerate the cardiac aging process through the receptor for advanced glycation end-products/transforming growth factor-β-Smad signaling pathway in cardiac fibroblasts.Loss of osteoglycin promotes angiogenesis in limb ischaemia mouse models via modulation of vascular endothelial growth factor and vascular endothelial growth factor receptor 2 signalling pathway.miR-22 in Smooth Muscle Cells: A Potential Therapy for Cardiovascular Disease.MicroRNA-22 Promotes Renal Tubulointerstitial Fibrosis by Targeting PTEN and Suppressing Autophagy in Diabetic Nephropathy.

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P2860

MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart.

http://www.wikidata.org/entity/Q36795205

description

2012 nî lūn-bûn

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

@zh-tw

2012年论文

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2012年论文

@zh

2012年论文

@zh-cn

name

MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart.

@ast

MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart.

@en

type

label

MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart.

@ast

MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart.

@en

prefLabel

MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart.

@ast

MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart.

@en

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MicroRNA-22 increases senescence and activates cardiac fibroblasts in the aging heart.

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P2093

Angelika Holzmann

http://www.w3.org/2001/XMLSchema#string

Annette Just

http://www.w3.org/2001/XMLSchema#string

Jan Fiedler

http://www.w3.org/2001/XMLSchema#string

Johann Bauersachs

http://www.w3.org/2001/XMLSchema#string

Paolo Galuppo

http://www.w3.org/2001/XMLSchema#string

Susanne Kneitz

http://www.w3.org/2001/XMLSchema#string

Thomas Thum

http://www.w3.org/2001/XMLSchema#string

Virginija Jazbutyte

http://www.w3.org/2001/XMLSchema#string

P2860

miR-17, miR-19b, miR-20a, and miR-106a are down-regulated in human aging

microRNA-22, downregulated in hepatocellular carcinoma and correlated with prognosis, suppresses cell proliferation and tumourigenicity

Integrated genomic approaches implicate osteoglycin (Ogn) in the regulation of left ventricular mass

MicroRNA: basic mechanisms and transcriptional regulatory networks for cell fate determination

Molecular cloning of a novel bone-forming compound: osteoinductive factor

MicroRNA-21 contributes to myocardial disease by stimulating MAP kinase signalling in fibroblasts

Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis

Expression studies of osteoglycin/mimecan (OGN) in the cochlea and auditory phenotype of Ogn-deficient mice

microRNA expression in the aging mouse lung.

De novo organ formation from differentiated cells: root nodule organogenesis.

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3

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35

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