Biblioteca Digital

923 resultados para MYOTUBE HYPERTROPHY

Peroxisome proliferator-activated receptor-α and NADPH oxidases interact to play an important regulatory role in pressure-overload cardiac hypertrophy.

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Does interaction between Peroxisome proliferator-activated receptor-α and NADPH oxidases play an important role in regulating pressure-overload cardiac hypertrophy?

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Cross-talk between NADPH oxidases and peroxisome proliferator-activated receptor-α differentially regulates left ventricular hypertrophy via specific activation of key signalling pathways.

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Investigation of mechanisms underlying the interaction between Nox2 NADPH oxidase and PPAR-α in left ventricular hypertrophy.

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The thiazolidinedione, troglitazone. does not initiate ventricular cardiomyocyte hypertrophy in vitro but may sensitise cardiomyocytes to the hypertrophic effects of serum growth factors

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CGRP and hypertrophy of cardiomyocytes

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Requirement for de novo synthesis of RNA and protein in endothelin-1 mediated cardiac hypertrophy

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Angiotensin II mediated hypertrophy involves activation of AT2 receptors and upregulation of creatine kinase

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The thiazolidinedione, troglitazone, does not initiate ventricular cardiomyocyte hypertrophy in vitro but may sensitise cardiomyocytes to the hypertrophic effects of serum growth factors

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Evidence for altered signalling mediated by ETB receptors in cardiomyocyte hypertrophy induced by pressure overload in spontaneously hypertensive rat.

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Altered functional responsiveness to neuropeptide Y acting at Y2 receptors in established ventricular cell hypertrophy in spontaneously hypertensive rat

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Altered responsiveness to beta2 adrenoceptor and NPY Y2 receptor stimulation during progression of cardiomyocyte hypertrophy

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ETB receptor involvement and associated mechanisms in endothelin-1 mediated hypertrophy in adult cardiomyocytes

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Increased potency of NPY to attenuate contraction via Y2 receptors during development of cardiomyocyte hypertrophy

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Evidence for enhanced endothelin ETB receptor affinity during the progression of hypertension-induced ventricular cardiomyocyte hypertrophy

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