Chapter title |
Studying the Role of AMPK in Cardiac Hypertrophy and Protein Synthesis
|
---|---|
Chapter number | 21 |
Book title |
AMPK
|
Published in |
Methods in molecular biology, January 2018
|
DOI | 10.1007/978-1-4939-7598-3_21 |
Pubmed ID | |
Book ISBNs |
978-1-4939-7597-6, 978-1-4939-7598-3
|
Authors |
Florence Mailleux, Christophe Beauloye, Jean-Luc Balligand, Sandrine Horman, Luc 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. |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
Unknown | 6 | 100% |
Demographic breakdown
Readers by professional status | Count | As % |
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Student > Bachelor | 1 | 17% |
Researcher | 1 | 17% |
Student > Doctoral Student | 1 | 17% |
Student > Master | 1 | 17% |
Unknown | 2 | 33% |
Readers by discipline | Count | As % |
---|---|---|
Biochemistry, Genetics and Molecular Biology | 1 | 17% |
Economics, Econometrics and Finance | 1 | 17% |
Materials Science | 1 | 17% |
Chemistry | 1 | 17% |
Unknown | 2 | 33% |