Therapeutic inhibition of fatty acid oxidation in right ventricular hypertrophy: exploiting Randle's cycle. - Wikidata - awgldk - TriplyDB

Therapeutic inhibition of fatty acid oxidation in right ventricular hypertrophy: exploiting Randle's cycle.

Therapeutic inhibition of fatty acid oxidation in right ventricular hypertrophy: exploiting Randle's cycle.

http://www.wikidata.org/entity/Q40096264

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Glycaemic control for patients with acute coronary syndrome Glycaemic control for patients with acute coronary syndrome Redox biology in pulmonary arterial hypertension (2013 Grover Conference Series)Cardiac energy metabolic alterations in pressure overload-induced left and right heart failure (2013 Grover Conference Series)The late Na+ current--origin and pathophysiological relevance 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.Emerging concepts in the molecular basis of pulmonary arterial hypertension: part I: metabolic plasticity and mitochondrial dynamics in the pulmonary circulation and right ventricle in pulmonary arterial hypertension Dynamin-related protein 1 (Drp1)-mediated diastolic dysfunction in myocardial ischemia-reperfusion injury: therapeutic benefits of Drp1 inhibition to reduce mitochondrial fission World Health Organization Group I Pulmonary Hypertension: Epidemiology and Pathophysiology.The right ventricle in pulmonary arterial hypertension: disorders of metabolism, angiogenesis and adrenergic signaling in right ventricular failure.Emerging Metabolic Therapies in Pulmonary Arterial Hypertension.Trimetazidine therapy for diabetic mouse hearts subjected to ex vivo acute heart failure.Lipid degradation promotes prostate cancer cell survival.New trial designs and potential therapies for pulmonary artery hypertension.Mechanisms of right heart failure-A work in progress and a plea for failure prevention Up-regulation of hexokinase1 in the right ventricle of monocrotaline induced pulmonary hypertension.Mitochondrial dynamics in pulmonary arterial hypertension.Severe pulmonary arterial hypertensive rats are tolerant to mild exercise.Right ventricular failure due to chronic pressure load: What have we learned in animal models since the NIH working group statement?Effects of ranolazine on exercise capacity, right ventricular indices, and hemodynamic characteristics in pulmonary arterial hypertension: a pilot study Severe pulmonary hypertension is associated with altered right ventricle metabolic substrate uptake Metabolomic analysis of bone morphogenetic protein receptor type 2 mutations in human pulmonary endothelium reveals widespread metabolic reprogramming.Standardized bioenergetic profiling of adult mouse cardiomyocytes.FOXO1-mediated upregulation of pyruvate dehydrogenase kinase-4 (PDK4) decreases glucose oxidation and impairs right ventricular function in pulmonary hypertension: therapeutic benefits of dichloroacetate The right ventricle: biologic insights and response to disease: updated.Reduced immunoreactivities of B-type natriuretic peptide in pulmonary arterial hypertension rats after ranolazine treatment Metabolic Dysfunction in Pulmonary Arterial Hypertension.Fatty Acid Metabolic Defects and Right Ventricular Lipotoxicity in Human Pulmonary Arterial Hypertension.Inhibition of fatty acid synthase is protective in pulmonary hypertension.Metabolism of the right ventricle and the response to hypertrophy and failure.Metabolic gene remodeling and mitochondrial dysfunction in failing right ventricular hypertrophy secondary to pulmonary arterial hypertension.Platelets from pulmonary hypertension patients show increased mitochondrial reserve capacity.Evidence for right ventricular lipotoxicity in heritable pulmonary arterial hypertension.Ranolazine: clinical applications and therapeutic basis.Anticipated classes of new medications and molecular targets for pulmonary arterial hypertension Treatment for pulmonary arterial hypertension-associated right ventricular dysfunction.Management of pulmonary hypertension due to heart failure with preserved ejection fraction.Fatty acid metabolism in pulmonary arterial hypertension: role in right ventricular dysfunction and hypertrophy.Mechanisms of Lipid Accumulation in the Bone Morphogenetic Protein Receptor Type 2 Mutant Right Ventricle.

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P2860

Therapeutic inhibition of fatty acid oxidation in right ventricular hypertrophy: exploiting Randle's cycle.

http://www.wikidata.org/entity/Q40096264

description

2011 nî lūn-bûn

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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2011年论文

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2011年论文

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name

Therapeutic inhibition of fatt ...... hy: exploiting Randle's cycle.

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Therapeutic inhibition of fatt ...... hy: exploiting Randle's cycle.

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Therapeutic inhibition of fatt ...... hy: exploiting Randle's cycle.

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S00109-011-0804-9

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Journal of Molecular Medicine

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Therapeutic inhibition of fatt ...... hy: exploiting Randle's cycle.

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P2093

Glenn Marsboom

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Jalees Rehman

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Lin Piao

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Peter Bache-Wiig

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Peter T Toth

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Stephen L Archer

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Yong-Hu Fang

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Zhigang Hong

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P2860

Trimetazidine. A review of its use in stable angina pectoris and other coronary conditions

The antianginal drug trimetazidine shifts cardiac energy metabolism from fatty acid oxidation to glucose oxidation by inhibiting mitochondrial long-chain 3-ketoacyl coenzyme A thiolase

Pharmacologic inhibition of fatty acid oxidation sensitizes human leukemia cells to apoptosis induction

Long-term effects of epoprostenol on the pulmonary vasculature in idiopathic pulmonary arterial hypertension.

Electrophysiological effects of ranolazine, a novel antianginal agent with antiarrhythmic properties.

Ranolazine decreases diastolic calcium accumulation caused by ATX-II or ischemia in rat hearts.

Partial fatty acid oxidation inhibitors for stable angina.

Ranolazine improves abnormal repolarization and contraction in left ventricular myocytes of dogs with heart failure by inhibiting late sodium current

Trimetazidine, a metabolic modulator, has cardiac and extracardiac benefits in idiopathic dilated cardiomyopathy.

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

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s00109-011-0804-9

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10.1007/S00109-011-0804-9

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1

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51602556

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21874543

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3249482

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