Loss of SMAD3 Promotes Vascular Remodeling in Pulmonary Arterial Hypertension via MRTF Disinhibition (scientific article published on 2 November 2017)

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Molecular regulation of vascular smooth muscle cell differentiation in development and disease

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Selective loss of TGFbeta Smad-dependent signalling prevents cell cycle arrest and promotes invasion in oesophageal adenocarcinoma cell lines

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Fate-determining mechanisms in epithelial-myofibroblast transition: major inhibitory role for Smad3

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Clinical and molecular genetic features of pulmonary hypertension in patients with hereditary hemorrhagic telangiectasia.

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Familial primary pulmonary hypertension (gene PPH1) is caused by mutations in the bone morphogenetic protein receptor-II gene

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Mutation in the gene for bone morphogenetic protein receptor II as a cause of primary pulmonary hypertension in a large kindred

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Chronic pulmonary artery pressure elevation is insufficient to explain right heart failure.

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Endoglin germline mutation in a patient with hereditary haemorrhagic telangiectasia and dexfenfluramine associated pulmonary arterial hypertension

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Cellular and molecular pathobiology of pulmonary arterial hypertension

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Selective enhancement of endothelial BMPR-II with BMP9 reverses pulmonary arterial hypertension.

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In Pulmonary Arterial Hypertension, Reduced BMPR2 Promotes Endothelial-to-Mesenchymal Transition via HMGA1 and Its Target Slug

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SMAD1 deficiency in either endothelial or smooth muscle cells can predispose mice to pulmonary hypertension

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Reduced BMPR2 expression induces GM-CSF translation and macrophage recruitment in humans and mice to exacerbate pulmonary hypertension

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Smaddening Complexity: The Role of Smad3 in Epithelial-Myofibroblast Transition

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Adaptation and remodelling of the pulmonary circulation in pulmonary hypertension

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β-catenin and Smad3 regulate the activity and stability of myocardin-related transcription factor during epithelial-myofibroblast transition

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Smad3 protein levels are modulated by Ras activity and during the cell cycle to dictate transforming growth factor-beta responses

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Sphingosine 1-phosphate elicits RhoA-dependent proliferation and MRTF-A mediated gene induction in CPCs

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Transforming growth factor-{beta}-inducible phosphorylation of Smad3

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Epithelial to mesenchymal transition in Madin-Darby canine kidney cells is accompanied by down-regulation of Smad3 expression, leading to resistance to transforming growth factor-beta-induced growth arrest.

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Microsatellite instability of endothelial cell growth and apoptosis genes within plexiform lesions in primary pulmonary hypertension

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Reciprocal expression of MRTF-A and myocardin is crucial for pathological vascular remodelling in mice.

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Alteration of transforming growth factor-beta1 response involves down-regulation of Smad3 signaling in myofibroblasts from skin fibrosis

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Primary pulmonary hypertension is associated with reduced pulmonary vascular expression of type II bone morphogenetic protein receptor

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Regulation of Smad3 expression in bleomycin-induced pulmonary fibrosis: a negative feedback loop of TGF-beta signaling

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Regulation of smooth muscle alpha-actin expression and hypertrophy in cultured mesangial cells

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Transforming growth factor-beta receptor mutations and pulmonary arterial hypertension in childhood

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Altered bone morphogenetic protein and transforming growth factor-beta signaling in rat models of pulmonary hypertension: potential for activin receptor-like kinase-5 inhibition in prevention and progression of disease

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Translating Research into Improved Patient Care in Pulmonary Arterial Hypertension

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Heterozygous germline mutations in BMPR2, encoding a TGF-beta receptor, cause familial primary pulmonary hypertension

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P433

issue

P407

language of work or name

English

Q1860

P921

main subject

microvasculature remodeling

Q6840464

P304

page(s)

244-260

P577

publication date

2017-11-02

P1433

published in

American Journal of Respiratory and Critical Care Medicine

Q4744267

P1476

title

Loss of SMAD3 Promotes Vascular Remodeling in Pulmonary Arterial Hypertension via MRTF Disinhibition

P478

volume

197

Reverse relations

cites work (P2860)

Q45071718	A Switch in TGF-β Signaling Explains Contradictory Findings in Pulmonary Arterial Hypertension
Q91879175	BMPR2 acts as a gatekeeper to protect endothelial cells from increased TGFβ responses and altered cell mechanics
Q64087821	Erratum: Loss of SMAD3 Promotes Vascular Remodeling in Pulmonary Arterial Hypertension via MRTF Disinhibition
Q91691135	Gefitinib-coated balloon inhibits the excessive hyperplasia of intima after vascular injuries through PI3K/AKT pathway
Q92149420	Hypoxia-responsive miRNA-21-5p inhibits Runx2 suppression by targeting SMAD7 in MC3T3-E1 cells
Q57066646	Inhibitory Antibodies against Activin A and TGF-β Reduce Self-Supported, but Not Soluble Factors-Induced Growth of Human Pulmonary Arterial Vascular Smooth Muscle Cells in Pulmonary Arterial Hypertension
Q64109638	Long non-coding RNA CASC2 suppresses pulmonary artery smooth muscle cell proliferation and phenotypic switch in hypoxia-induced pulmonary hypertension
Q61810180	Pathology and pathobiology of pulmonary hypertension: state of the art and research perspectives
Q57476151	SRF'ing and SAP'ing - the role of MRTF proteins in cell migration
Q64098812	Schistosome infection and its effect on pulmonary circulation
Q60047435	SphK1/S1P mediates TGF-β1-induced proliferation of pulmonary artery smooth muscle cells and its potential mechanisms
Q57166510	TGF-β and BMPR2 Signaling in PAH: Two Black Sheep in One Family
Q88039560	Update in Pulmonary Vascular Disease 2016 and 2017

P356	DOI	10.1164/RCCM.201702-0386OC
P698	PubMed publication ID	29095649