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Smooth muscle phenotypic modulation is an early event in aortic aneurysms

Smooth muscle phenotypic modulation is an early event in aortic aneurysms

http://www.wikidata.org/entity/Q30434473

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Mutations in myosin light chain kinase cause familial aortic dissections MicroRNA-26a is a novel regulator of vascular smooth muscle cell function MicroRNAs: Novel Players in Aortic Aneurysm Potential contribution of phenotypically modulated smooth muscle cells and related inflammation in the development of experimental obstructive pulmonary vasculopathy in rats Aromatase is required for female abdominal aortic aneurysm protection.B2 cells suppress experimental abdominal aortic aneurysms.KLF4 regulates abdominal aortic aneurysm morphology and deletion attenuates aneurysm formation Adenosine 2A receptor modulates inflammation and phenotype in experimental abdominal aortic aneurysms Genetic and pharmacologic disruption of interleukin-1β signaling inhibits experimental aortic aneurysm formation.Bone marrow-derived MCP1 required for experimental aortic aneurysm formation and smooth muscle phenotypic modulation.Development of a novel murine model of aortic aneurysms using peri-adventitial elastase.Smooth muscle cell-specific Notch1 haploinsufficiency restricts the progression of abdominal aortic aneurysm by modulating CTGF expression.Non-coding RNA Contribution to Thoracic and Abdominal Aortic Aneurysm Disease Development and Progression.IL-19 reduces ligation-mediated neointimal hyperplasia by reducing vascular smooth muscle cell activation.Molecular regulation of contractile smooth muscle cell phenotype: implications for vascular tissue engineering.Differential expression of Hedgehog/Notch and transforming growth factor-β in human abdominal aortic aneurysms.Cyclooxygenase-2 inhibition attenuates abdominal aortic aneurysm progression in hyperlipidemic mice.Assessment of elastase-induced murine abdominal aortic aneurysms: comparison of ultrasound imaging with in situ video microscopy.Repression of Sox9 by Jag1 is continuously required to suppress the default chondrogenic fate of vascular smooth muscle cells.Resveratrol induces p53 and suppresses myocardin-mediated vascular smooth muscle cell differentiation.Generation of human vascular smooth muscle subtypes provides insight into embryological origin-dependent disease susceptibility Effect of glucose on the biomechanical function of arterial elastin Acute mechanical effects of elastase on the infrarenal mouse aorta: implications for models of aneurysms.Three-dimensional microstructural changes in murine abdominal aortic aneurysms quantified using immunofluorescent array tomography.Pelvic Organ Support in Animals with Partial Loss of Fibulin-5 in the Vaginal Wall.Epigenetic regulation of smooth muscle cell plasticity.Vascular smooth muscle cell phenotypic plasticity: focus on chromatin remodelling.Inhibition of Proteasome Activity by Low-dose Bortezomib Attenuates Angiotensin II-induced Abdominal Aortic Aneurysm in Apo E(-/-) Mice.Thoracic aortic aneurysm (TAAD)-causing mutation in actin affects formin regulation of polymerization.Resident phenotypically modulated vascular smooth muscle cells in healthy human arteries.Aneurysm miRNA Signature Differs, Depending on Disease Localization and Morphology Perivascular cells in blood vessel regeneration.Slug Is Increased in Vascular Remodeling and Induces a Smooth Muscle Cell Proliferative Phenotype.Exploring smooth muscle phenotype and function in a bioreactor model of abdominal aortic aneurysm Inhibition of Receptor-Interacting Protein Kinase 1 with Necrostatin-1s ameliorates disease progression in elastase-induced mouse abdominal aortic aneurysm model.The vascular smooth muscle cell: a therapeutic target in Type 2 diabetes?Gene Expression Profiling in Abdominal Aortic Aneurysms After Finite Element Rupture Risk Assessment.Upregulation of MicroRNA-15a Contributes to Pathogenesis of Abdominal Aortic Aneurysm (AAA) by Modulating the Expression of Cyclin-Dependent Kinase Inhibitor 2B (CDKN2B).DNA methylome analysis reveals distinct epigenetic patterns of ascending aortic dissection and bicuspid aortic valve.Inhibition of the mTOR pathway in abdominal aortic aneurysm: implications of smooth muscle cell contractile phenotype, inflammation, and aneurysm expansion.

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Smooth muscle phenotypic modulation is an early event in aortic aneurysms

http://www.wikidata.org/entity/Q30434473

description

2009 nî lūn-bûn

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2009 թուականի Դեկտեմբերին հրատարակուած գիտական յօդուած

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2009 թվականի դեկտեմբերին հրատարակված գիտական հոդված

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2009年の論文

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2009年論文

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2009年論文

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2009年論文

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2009年论文

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name

Smooth muscle phenotypic modulation is an early event in aortic aneurysms

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Smooth muscle phenotypic modulation is an early event in aortic aneurysms

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Smooth muscle phenotypic modulation is an early event in aortic aneurysms

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Smooth muscle phenotypic modulation is an early event in aortic aneurysms

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Smooth muscle phenotypic modulation is an early event in aortic aneurysms

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J.JTCVS.2009.07.075

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The Journal of Thoracic and Cardiovascular Surgery

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Smooth muscle phenotypic modulation is an early event in aortic aneurysms

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Christine L Lau

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Christopher W Moehle

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Gary K Owens

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Hong Pei

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Sandra P Walton

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Zequan Yang

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P2860

Losartan, an AT1 antagonist, prevents aortic aneurysm in a mouse model of Marfan syndrome

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

Regulation of smooth muscle alpha-actin expression in vivo is dependent on CArG elements within the 5' and first intron promoter regions.

Similarities and differences in smooth muscle alpha-actin induction by TGF-beta in smooth muscle versus non-smooth muscle cells.

CArG elements control smooth muscle subtype-specific expression of smooth muscle myosin in vivo

A G/C element mediates repression of the SM22alpha promoter within phenotypically modulated smooth muscle cells in experimental atherosclerosis.

Kruppel-like factor 4 abrogates myocardin-induced activation of smooth muscle gene expression.

Conditional deletion of Krüppel-like factor 4 delays downregulation of smooth muscle cell differentiation markers but accelerates neointimal formation following vascular injury

Multiple repressor pathways contribute to phenotypic switching of vascular smooth muscle cells.

MYH11 mutations result in a distinct vascular pathology driven by insulin-like growth factor 1 and angiotensin II

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