Suppression of histone deacetylases worsens right ventricular dysfunction after pulmonary artery banding in rats. - Wikidata - wikimedia - TriplyDB

Suppression of histone deacetylases worsens right ventricular dysfunction after pulmonary artery banding in rats.

Suppression of histone deacetylases worsens right ventricular dysfunction after pulmonary artery banding in rats.

http://www.wikidata.org/entity/Q44963004

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Mechanisms of Vascular Smooth Muscle Contraction and the Basis for Pharmacologic Treatment of Smooth Muscle Disorders Epigenetic modulation as a therapeutic approach for pulmonary arterial hypertension Right ventricular failure and pathobiology in patients with congenital heart disease - implications for long-term follow-up A comprehensive review: the evolution of animal models in pulmonary hypertension research; are we there yet?Right ventricular adaptation and failure in pulmonary arterial hypertension.The emerging role of epigenetics in pulmonary arterial hypertension: an important avenue for clinical trials (2015 Grover Conference Series)Emerging roles for histone deacetylases in pulmonary hypertension and right ventricular remodeling (2013 Grover Conference series)Acetyl-lysine erasers and readers in the control of pulmonary hypertension and right ventricular hypertrophy Human GRK4γ142V Variant Promotes Angiotensin II Type I Receptor-Mediated Hypertension via Renal Histone Deacetylase Type 1 Inhibition.A brief overview of mouse models of pulmonary arterial hypertension: problems and prospects.The cancer theory of pulmonary arterial hypertension.Epigenetic modifications: basic mechanisms and role in cardiovascular disease (2013 Grover Conference series).Pharmacologic treatments for pulmonary hypertension: exploring pharmacogenomics Blocking the class I histone deacetylase ameliorates renal fibrosis and inhibits renal fibroblast activation via modulating TGF-beta and EGFR signaling Restoration of impaired endothelial myocyte enhancer factor 2 function rescues pulmonary arterial hypertension.Histone deacetylase inhibitors for treating a spectrum of diseases not related to cancer Potential non-oncological applications of histone deacetylase inhibitors.Epigenetic mechanisms of pulmonary hypertension.Right ventricular failure due to chronic pressure load: What have we learned in animal models since the NIH working group statement?Mitochondria and Oxidative Stress in the Cardiorenal Metabolic Syndrome.Pulmonary artery smooth muscle cell proliferation and migration in fetal lambs acclimatized to high-altitude long-term hypoxia: role of histone acetylation MLL histone methylases regulate expression of HDLR-SR-B1 in presence of estrogen and control plasma cholesterol in vivo Novel therapeutic approaches to preserve the right ventricle.Histone deacetylase inhibitors (HDACIs): multitargeted anticancer agents The role of redox signaling in epigenetics and cardiovascular disease.Integrating molecular genetics and systems approaches to pulmonary vascular diseases.Selective class I histone deacetylase inhibition suppresses hypoxia-induced cardiopulmonary remodeling through an antiproliferative mechanism.Right Ventricular Myocardial Stiffness in Experimental Pulmonary Arterial Hypertension: Relative Contribution of Fibrosis and Myofibril Stiffness.Histone deacetylation contributes to low extracellular superoxide dismutase expression in human idiopathic pulmonary arterial hypertension.Metabolic gene remodeling and mitochondrial dysfunction in failing right ventricular hypertrophy secondary to pulmonary arterial hypertension.Mechanical regulation of epigenetics in vascular biology and pathobiology Transcription factors, transcriptional coregulators, and epigenetic modulation in the control of pulmonary vascular cell phenotype: therapeutic implications for pulmonary hypertension (2015 Grover Conference series).Epigenetic Regulation of Interleukin 6 by Histone Acetylation in Macrophages and Its Role in Paraquat-Induced Pulmonary Fibrosis.Update in pulmonary vascular diseases 2011.Epigenetics within the matrix: a neo-regulator of fibrotic disease.Anticipated classes of new medications and molecular targets for pulmonary arterial hypertension Molecular basis of organ fibrosis: potential therapeutic approaches.From cell phenotype to epigenetic mechanisms: new insights into regenerating myocardium.Novel and emerging therapies for pulmonary hypertension.Pressure-overload-induced right heart failure.

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P2860

Suppression of histone deacetylases worsens right ventricular dysfunction after pulmonary artery banding in rats.

http://www.wikidata.org/entity/Q44963004

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2011 nî lūn-bûn

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2011年学术文章

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Suppression of histone deacety ...... monary artery banding in rats.

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Suppression of histone deacety ...... monary artery banding in rats.

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Suppression of histone deacety ...... monary artery banding in rats.

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Suppression of histone deacety ...... monary artery banding in rats.

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Suppression of histone deacety ...... monary artery banding in rats.

@en

Suppression of histone deacety ...... monary artery banding in rats.

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RCCM.201007-1106OC

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American Journal of Respiratory and Critical Care Medicine

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Suppression of histone deacety ...... monary artery banding in rats.

@en

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Antonio Abbate

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Ayser A Al Hussaini

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Donatas Kraskauskas

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Harm J Bogaard

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Michael Kasper

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Norbert F Voelkel

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Shiro Mizuno

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P2860

Histone deacetylase inhibition reduces myocardial ischemia-reperfusion injury in mice

Hdac2 regulates the cardiac hypertrophic response by modulating Gsk3 beta activity

Pitx2c and Nkx2-5 are required for the formation and identity of the pulmonary myocardium

Histone and chromatin cross-talk

Cardiac fibroblasts are essential for the adaptive response of the murine heart to pressure overload.

Apoptotic and autophagic cell death induced by histone deacetylase inhibitors.

Suppression of class I and II histone deacetylases blunts pressure-overload cardiac hypertrophy.

Control of cardiac growth by histone acetylation/deacetylation.

Collagen remodeling of the pressure-overloaded, hypertrophied nonhuman primate myocardium.

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

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Ramesh Natarajan

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49813383

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