Studying the Role of AMPK in Cardiac Hypertrophy and Protein Synthesis

Methods in Molecular Biology
Florence MailleuxLuc Bertrand

Abstract

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.

Citations

Jan 14, 2021·Biochemical Society Transactions·Hongyang ShuDao Wen Wang
Oct 14, 2020·Cell Biology International·Jiantao QiuXueying Tan
Apr 27, 2021·Oxidative Medicine and Cellular Longevity·Karan Naresh AminRamkumar Kunka Mohanram

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