Abstract
Metabolic syndrome has been widely associated with an increased risk for acute cardiovascular events. Emerging evidence supports metabolic syndrome as a condition favoring an adverse cardiac remodeling, which might evolve towards heart dysfunction and failure. This pathological remodeling has been described to result from the cardiac adaptive response to clinical mechanical conditions (such as hypertension, dyslipidemia, and hyperglycemia), soluble inflammatory molecules (such as cytokines and chemokines), as well as hormones (such as insulin), characterizing the pathophysiology of metabolic syndrome. Moreover, these cardiac processes (resulting in cardiac hypertrophy and fibrosis) are also associated with the modulation of intracellular signalling pathways within cardiomyocytes. Amongst the different intracellular kinases, mitogen-activated protein kinases (MAPKs) were shown to be involved in heart damage in metabolic syndrome. However, their role remains controversial. In this paper, we will discuss and update evidence on MAPK-mediated mechanisms underlying cardiac adverse remodeling associated with metabolic syndrome.
Highlights
E prevalence of metabolic syndrome is rapidly increasing in the western world [1]
Not speci cally performed in models of metabolic syndrome, in vitro studies using isolated cardiomyocytes have shown that mitogen-activated protein kinases (MAPKs) might be involved in cardiac hypertrophy via three traditional phases (i) the activation of speci c transmembrane proteins; (ii) intracellular signal transduction; (iii) the activation of cytosolic and nuclear events [12]
Since cardiac hypertrophy is characterized by increased cell size, it has been suggested that MAPKs might play a critical role in cardiac remodeling in hypertensive patients with metabolic syndrome. is appears to be achieved by modulating the activity of numerous transcription factors that target speci c genes involved in structural response of the myocardium
Summary
E prevalence of metabolic syndrome is rapidly increasing in the western world [1]. Metabolic syndrome has been de ned as a cluster of multiple disorders including insulin resistance, abdominal obesity, dyslipidemia, increased blood pressure, hypercholesterolemia, and proin ammatory state [2]. Several de nitions have been historically proposed during the last decades, including oxidative stress, leptin resistances and endothelial dysfunction as key pathophysiological mechanisms contributing to the increase of cardiovascular risk that affect metabolic syndrome patients [2, 3]. Sustained overload leads to maladaptive and detrimental remodeling, as reported in detail by Buckberg and coworkers [9] These studies suggest that cardiac remodeling in metabolic syndrome depends on the different component disorders and might not be a disease per se but rather an adaptive response. Since cardiac hypertrophy is characterized by increased cell size, it has been suggested that MAPKs might play a critical role in cardiac remodeling in hypertensive patients with metabolic syndrome. We will provide an overview on the role of MAPKs in the adverse cardiac remodeling that is associated with metabolic syndrome
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