Mailleux Florence, Beauloye Christophe, Balligand Jean-Luc, Horman Sandrine, Bertrand Luc
Pole of Cardiovascular Research, Institut de Recherche Expérimentale et Clinique, Université catholique de Louvain, Brussels, Belgium.
Division of Cardiology, Cliniques Universitaires Saint-Luc, Brussels, Belgium.
Methods Mol Biol. 2018;1732:321-342. doi: 10.1007/978-1-4939-7598-3_21.
Pathological cardiac hypertrophy, which is a compensatory mechanism established to maintain cardiac function in response to neurohormonal or mechanical stresses, becomes maladaptive with time and frequently leads to heart failure. AMP-activated protein kinase (AMPK) has been extensively described in the literature to act as a break in cardiac hypertrophy development. Its anti-hypertrophic action mostly correlates with the inhibition of several important players of cardiac hypertrophy including protein synthesis and pro-hypertrophic gene expression pathways involving the transcription factor nuclear factor of activated T cells (NFAT) and the mitogen-activated protein kinases ERK1/2. In this chapter, we describe methodologies designed to evaluate cardiomyocyte hypertrophy and its major molecular mechanisms in response to AMPK activation. Two different compounds, AICAr and the biguanide phenformin, were used to promote AMPK activation.
病理性心脏肥大是一种为应对神经激素或机械应激而建立的维持心脏功能的代偿机制，但随着时间的推移会变得适应不良，并常常导致心力衰竭。文献中已广泛描述了AMP激活的蛋白激酶（AMPK）在心脏肥大发展过程中起到刹车作用。其抗肥大作用主要与抑制心脏肥大的几个重要参与者有关，包括蛋白质合成以及涉及转录因子活化T细胞核因子（NFAT）和丝裂原活化蛋白激酶ERK1/2的促肥大基因表达途径。在本章中，我们描述了旨在评估心肌细胞肥大及其对AMPK激活反应的主要分子机制的方法。使用了两种不同的化合物，AICAr和双胍类药物苯乙双胍来促进AMPK激活。
