Role of Mitogen-Activated Protein Kinase Pathways in Multifactorial Adverse Cardiac Remodeling Associated with Metabolic Syndrome

Figure 1

Intracellular pathways mediating hypertrophic cardiac remodelling in metabolic syndrome. Intracellular pathways mediated by phosphatidylinositol 3-kinase (PI3-K) activation play a pivotal role in insulin-mediated glucose transport in cardiomyocytes. Metabolic syndrome is associated with impaired intracellular signaling that could be activated by various stimuli, including inflammatory cytokines. These pathways, mainly dependent on MAPK activation (composed of extracellular signal-regulated kinase [ERK], c-Jun N-terminal kinase [JNK], and p38 MAPK), could be also triggered by chirurgical manipulation (such as transverse aortic constriction [TAC]). MAPK activation might be considered as a critical mechanism aggravating cardiac hypertrophy as well as cardiomyocyte insulin resistance in metabolic syndrome.