Adaptive and maladptive effects of SMAD3 signaling in the adult heart after hemodynamic pressure overloading - Test2 - elhamkhani - TriplyDB

Adaptive and maladptive effects of SMAD3 signaling in the adult heart after hemodynamic pressure overloading

Adaptive and maladptive effects of SMAD3 signaling in the adult heart after hemodynamic pressure overloading

http://www.wikidata.org/entity/Q34722251

about

The function of miRNA in cardiac hypertrophy Cardiac-specific mindin overexpression attenuates cardiac hypertrophy via blocking AKT/GSK3β and TGF-β1-Smad signalling.Cardiac myocyte-specific ablation of follistatin-like 3 attenuates stress-induced myocardial hypertrophy.Circulating microRNA expression profile and systemic right ventricular function in adults after atrial switch operation for complete transposition of the great arteries.Coordinated regulation of extracellular matrix synthesis by the microRNA-29 family in the trabecular meshwork Exendin-4 protects against post-myocardial infarction remodelling via specific actions on inflammation and the extracellular matrix The development of myocardial fibrosis in transgenic mice with targeted overexpression of tumor necrosis factor requires mast cell-fibroblast interactions.Smad-mediated regulation of microRNA biosynthesis.Cardiomyocyte overexpression of miR-27b induces cardiac hypertrophy and dysfunction in mice Transforming growth factor beta signaling in adult cardiovascular diseases and repair.Cardiac lineage protein-1 (CLP-1) regulates cardiac remodeling via transcriptional modulation of diverse hypertrophic and fibrotic responses and angiotensin II-transforming growth factor β (TGF-β1) signaling axis.Genetic deficiency of Smad3 protects the kidneys from atrophy and interstitial fibrosis in 2K1C hypertension.Variable phenotype in murine transverse aortic constriction.Reduced endoglin activity limits cardiac fibrosis and improves survival in heart failure.Angiotensin receptor type 1 single nucleotide polymorphism 1166A/C is associated with malignant arrhythmias and altered circulating miR-155 levels in patients with chronic heart failure.Myocyte-fibroblast communication in cardiac fibrosis and arrhythmias: Mechanisms and model systems.Bone marrow mesenchymal stem cells for post-myocardial infarction cardiac repair: microRNAs as novel regulators.Heat shock transcription factor 1 protects against pressure overload-induced cardiac fibrosis via Smad3.MicroRNAs--regulators of signaling networks in dilated cardiomyopathy.MicroRNA epigenetics: a new avenue for wound healing research.Clinical applications of miRNAs in cardiac remodeling and heart failure Role of microRNAs in cardiac remodeling and heart failure.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.Arjunolic Acid, a Peroxisome Proliferator-Activated Receptor Alpha Agonist Regresses Cardiac Fibrosis by Inhibiting Non-canonical TGF-β Signaling.Comparative Analyses of MicroRNA Microarrays during Cardiogenesis: Functional Perspectives.Cardiac epithelial-mesenchymal transition is blocked by monomethylarsonous acid (III)MicroRNA-29: A Crucial Player in Fibrotic Disease.The p21-activated kinase 1 (Pak1) signalling pathway in cardiac disease: from mechanistic study to therapeutic exploration.The microRNA-15 family inhibits the TGFβ-pathway in the heart.Connexin and fibrosis related microRNAs in complex fractionated atrial electrograms.Pivotal role of cardiomyocyte TGF-β signaling in the murine pathological response to sustained pressure overload.Cardiac pathologies in relation to Smad-dependent pathways.Angiotensin II induced differentially expressed microRNAs in adult rat cardiac fibroblasts.Fibroblast-specific TGF-β-Smad2/3 signaling underlies cardiac fibrosis.Cardiovascular phenotype in Smad3 deficient mice with renovascular hypertension.The Role of c-SKI in Regulation of TGFβ-Induced Human Cardiac Fibroblast Proliferation and ECM Protein Expression.Rosmarinic acid attenuates cardiac fibrosis following long-term pressure overload via AMPKα/Smad3 signaling.A myriad of roles of miR-25 in health and disease.

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P2860

Adaptive and maladptive effects of SMAD3 signaling in the adult heart after hemodynamic pressure overloading

http://www.wikidata.org/entity/Q34722251

description

2009 nî lūn-bûn

@nan

2009 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2009 թվականի սեպտեմբերին 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年論文

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2009年論文

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2009年论文

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name

Adaptive and maladptive effect ...... modynamic pressure overloading

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Adaptive and maladptive effect ...... modynamic pressure overloading

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Adaptive and maladptive effect ...... modynamic pressure overloading

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Adaptive and maladptive effect ...... modynamic pressure overloading

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Adaptive and maladptive effect ...... modynamic pressure overloading

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Adaptive and maladptive effect ...... modynamic pressure overloading

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CIRCHEARTFAILURE.108.823070

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Circulation: Heart Failure

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Adaptive and maladptive effect ...... modynamic pressure overloading

@en

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Julia Adrogue

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

Mark L Entman

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

Masakuni Ishiyama

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

Natarajan Sivasubramanian

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

Sandra Haudek

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Vijay Divakaran

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P2860

Analysis of Relative Gene Expression Data Using Real-Time Quantitative PCR and the 2−ΔΔCT Method

Smad-dependent and Smad-independent pathways in TGF-beta family signalling

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

Collagen fibril formation

SMAD proteins control DROSHA-mediated microRNA maturation

Transcriptional control by the TGF-beta/Smad signaling system

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

Load-dependent and -independent regulation of proinflammatory cytokine and cytokine receptor gene expression in the adult mammalian heart.

Interplay of matrix metalloproteinases, tissue inhibitors of metalloproteinases and their regulators in cardiac matrix remodeling.

Gene expression in fibroblasts and fibrosis: involvement in cardiac hypertrophy.

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633-642

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10.1161/CIRCHEARTFAILURE.108.823070

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6

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2

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Douglas L. Mann

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2009-09-24T00:00:00Z

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38095802

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19919989

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3064555

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