Angiotensin II-induced cardiomyocyte hypertrophy in vitro is TAK1-dependent and Smad2/3-independent. (Q54551007)

31 May 2018

title

Angiotensin II-induced cardiomyocyte hypertrophy in vitro is TAK1-dependent and Smad2/3-independent. (English)

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31 May 2018

author

Helen M. Arthur

5

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author name string

Sarah J Watkins

1

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Gillian M Borthwick

2

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Rachael Oakenfull

3

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Andrew Robson

4

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publication date

10 November 2011

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31 May 2018

published in

Hypertension Research

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volume

35

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page(s)

393-398

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issue

4

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https://scigraph.springernature.com/pub.10.1038/hr.2011.196

exact match

0 references

cites work

TGF-beta1 and angiotensin networking in cardiac remodeling

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Molecular characterization of angiotensin II--induced hypertrophy of cardiac myocytes and hyperplasia of cardiac fibroblasts. Critical role of the AT1 receptor subtype

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Transforming growth factor (TGF)-β signaling in cardiac remodeling.

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The role of TGF-beta signaling in myocardial infarction and cardiac remodeling

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TGF-beta1 mediates the hypertrophic cardiomyocyte growth induced by angiotensin II.

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TGFbeta-SMAD signal transduction: molecular specificity and functional flexibility

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TAK1, but not TAB1 or TAB2, plays an essential role in multiple signaling pathways in vivo

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7 January 2021

TAK1 is activated in the myocardium after pressure overload and is sufficient to provoke heart failure in transgenic mice.

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A direct interaction between TGFbeta activated kinase 1 and the TGFbeta type II receptor: implications for TGFbeta signalling and cardiac hypertrophy

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Rapid transcriptional activation and early mRNA turnover of brain natriuretic peptide in cardiocyte hypertrophy. Evidence for brain natriuretic peptide as an "emergency" cardiac hormone against ventricular overload

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The H9C2 cell line and primary neonatal cardiomyocyte cells show similar hypertrophic responses in vitro

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SB-431542 is a potent and specific inhibitor of transforming growth factor-beta superfamily type I activin receptor-like kinase (ALK) receptors ALK4, ALK5, and ALK7

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Activin receptor-like kinase (ALK)1 is an antagonistic mediator of lateral TGFbeta/ALK5 signaling

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Calsarcin-1 protects against angiotensin-II induced cardiac hypertrophy

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Peroxisome proliferator-activated receptor beta/delta activation improves angiotensin II-induced cardiac hypertrophy in vitro

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Cardiac hypertrophy induced by mitogen-activated protein kinase kinase 7, a specific activator for c-Jun NH2-terminal kinase in ventricular muscle cells

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TGF-beta1 induces cardiac hypertrophic responses via PKC-dependent ATF-2 activation

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Tumor necrosis factor receptor-associated factor-6 and ribosomal S6 kinase intracellular pathways link the angiotensin II AT1 receptor to the phosphorylation and activation of the IkappaB kinase complex in vascular smooth muscle cells

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Angiotensin II induces connective tissue growth factor and collagen I expression via transforming growth factor-beta-dependent and -independent Smad pathways: the role of Smad3

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Pivotal role of cardiomyocyte TGF-β signaling in the murine pathological response to sustained pressure overload

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Cardiac fibrosis in mice with hypertrophic cardiomyopathy is mediated by non-myocyte proliferation and requires Tgf-β.

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Targeted disruption of Smad4 in cardiomyocytes results in cardiac hypertrophy and heart failure

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Targeted inhibition of activin receptor-like kinase 5 signaling attenuates cardiac dysfunction following myocardial infarction

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In vivo RNAi-mediated silencing of TAK1 decreases inflammatory Th1 and Th17 cells through targeting of myeloid cells.

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7 January 2021

Identifiers

DOI

10.1038/HR.2011.196

1 reference

31 May 2018

Dimensions Publication ID

0 references

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31 May 2018