The opposing effects of CCN2 and CCN5 on the development of cardiac hypertrophy and fibrosis. - Wikidata - awgldk - TriplyDB

The opposing effects of CCN2 and CCN5 on the development of cardiac hypertrophy and fibrosis.

The opposing effects of CCN2 and CCN5 on the development of cardiac hypertrophy and fibrosis.

http://www.wikidata.org/entity/Q34112864

about

Eyeing the Cyr61/CTGF/NOV (CCN) group of genes in development and diseases: highlights of their structural likenesses and functional dissimilarities Cross talk between cardiac myocytes and fibroblasts: from multiscale investigative approaches to mechanisms and functional consequences Taking aim at the extracellular matrix: CCN proteins as emerging therapeutic targets AAV-mediated knock-down of HRC exacerbates transverse aorta constriction-induced heart failure Expression profile of matricellular proteins in hypertrophied right ventricle of monocrotaline-induced pulmonary hypertensive rats.Spatial-temporal modulation of CCN proteins during wound healing in human skin in vivo.Assessment of cardiovascular fibrosis using novel fluorescent probes.Genome-wide RNA-Sequencing analysis identifies a distinct fibrosis gene signature in the conjunctiva after glaucoma surgery Long-term in vivo resistin overexpression induces myocardial dysfunction and remodeling in rats.A new model of congestive heart failure in rats.Matricellular proteins in cardiac adaptation and disease.Genetic Analysis of Connective Tissue Growth Factor as an Effector of Transforming Growth Factor β Signaling and Cardiac Remodeling.CCN5 attenuates profibrotic phenotypes of fibroblasts through the Smad6-CCN2 pathway: Potential role in epidural ﬁbrosis.CTGF/CCN2 Postconditioning Increases Tolerance of Murine Hearts towards Ischemia-Reperfusion Injury.CCN2/CTGF regulates neovessel formation via targeting structurally conserved cystine knot motifs in multiple angiogenic regulators.Connective tissue growth factor regulates cardiac function and tissue remodeling in a mouse model of dilated cardiomyopathy Connective tissue growth factor regulates retinal neovascularization through p53 protein-dependent transactivation of the matrix metalloproteinase (MMP)-2 gene Extracellular matrix and fibroblast communication following myocardial infarction.Matricellular protein CCN1 promotes regression of liver fibrosis through induction of cellular senescence in hepatic myofibroblasts.Muscle ring finger 1 and muscle ring finger 2 are necessary but functionally redundant during developmental cardiac growth and regulate E2F1-mediated gene expression in vivo.ERK1/2 directly acts on CTGF/CCN2 expression to mediate myocardial fibrosis in cardiomyopathy caused by mutations in the lamin A/C gene Changes in cardiac structure and function in a modified rat model of myocardial hypertrophy.Possible strategies for anti-fibrotic drug intervention in scleroderma.Importance of myocyte-nonmyocyte interactions in cardiac development and disease Role of the Wnt-Frizzled system in cardiac pathophysiology: a rapidly developing, poorly understood area with enormous potential.Contributions of cardiomyocyte-cardiac fibroblast-immune cell interactions in heart failure development.Regulatory RNAs and paracrine networks in the heart.Cellular Interplay between Cardiomyocytes and Nonmyocytes in Cardiac Remodeling.Involvement of multiple CCN family members in platelets that support regeneration of joint tissues.Matricellular Protein CCN5 Reverses Established Cardiac Fibrosis.Fibroblast-Extracellular Matrix Interactions in Tissue Fibrosis Anti-fibrotic effect of CCN3 accompanied by altered gene expression profile of the CCN family Evaluation of circulating levels of CCN2/connective tissue growth factor in patients with ST-elevation myocardial infarction.CCN2: a bona fide target for anti-fibrotic drug intervention CCN2 induces cellular senescence in fibroblasts.Mitochondrial quality-control dysregulation in conditional HO-1-/- mice.Yin and Yang Part Deux: CCN5 inhibits the pro-fibrotic effects of CCN2 Pivotal role of cardiomyocyte TGF-β signaling in the murine pathological response to sustained pressure overload.Cardiac myocyte β3-adrenergic receptors prevent myocardial fibrosis by modulating oxidant stress-dependent paracrine signaling.CCN5/WISP2 and metabolic diseases.

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The opposing effects of CCN2 and CCN5 on the development of cardiac hypertrophy and fibrosis.

http://www.wikidata.org/entity/Q34112864

description

2010 nî lūn-bûn

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2010 թուականի Ապրիլին հրատարակուած գիտական յօդուած

@hyw

2010 թվականի ապրիլին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

The opposing effects of CCN2 a ...... diac hypertrophy and fibrosis.

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The opposing effects of CCN2 a ...... diac hypertrophy and fibrosis.

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The opposing effects of CCN2 a ...... diac hypertrophy and fibrosis.

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The opposing effects of CCN2 a ...... diac hypertrophy and fibrosis.

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The opposing effects of CCN2 a ...... diac hypertrophy and fibrosis.

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The opposing effects of CCN2 a ...... diac hypertrophy and fibrosis.

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The opposing effects of CCN2 a ...... diac hypertrophy and fibrosis.

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The opposing effects of CCN2 a ...... diac hypertrophy and fibrosis.

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The opposing effects of CCN2 a ...... diac hypertrophy and fibrosis.

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J.YJMCC.2010.04.010

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Journal of Molecular and Cellular Cardiology

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The opposing effects of CCN2 a ...... diac hypertrophy and fibrosis.

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Bo Youn Choi

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Dong Kwon Yang

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Dongtak Jeong

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Hyeseon Cha

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Jooyeon Kim

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Min-Ah Lee

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Moon Hee Jeong

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Pyoung Oh Yoon

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Roger J Hajjar

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Seung Pil Jang

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294-303

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scholarly article

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10.1016/J.YJMCC.2010.04.010

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2

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49

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2010-04-27T00:00:00Z

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20430035

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