The term “ventricular remodeling” refers to changes in left ventricule structure in response to haemodynamic stress such as myocardial infarction (MI). After MI, this response initially compensates the loss of contractile mass. However, maladaptative processes progressively develop and increase the risk for the development of heart failure and premature death. The pathological transition is multifactorial and non muscle cells residing in the interstitium such as cardiac fibroblasts (CF) are important players in HF. CF predominantly express the α1 catalytic subunit of AMP-activated protein kinase (AMPKα1). This thesis aims at further substantiating the role of this AMPK isoform in the pathogenesis of post-MI LV remodeling and more particularly in the regulation of fibrotic properties of CF. Our data genetically demonstrate the centrality of AMPKα1 in post-MI scar formation and highlight the specificity of this catalytic isoform in cardiac fibroblast/myofibroblast biology.
Noppe, G. (2015). Rôle de la protéine kinase AMPK dans le développement de la fibrose au cours du remodelage ventriculaire gauche post-infarctus. https://hdl.handle.net/2078.5/192892