Campos VN, Rivas EE, Andrade RM

Language: Spanish
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ABSTRACT

Diabetes mellitus is a well-known risk factor for the development of heart failure. Several molecular mechanisms link diabetes to myocardial inflammation. It is known that in subjects with metabolic syndrome and type 2 diabetes, high glucose levels and dyslipidemia directly induce the positive regulation and secretion of cytokines, chemokines and adhesion molecules in cardiac cells by modulating multiple signaling pathways that converge towards nuclear factor kappa-light chain-enhancer of activated B cells. The activation of the renin-angiotensin-aldosterone system, the accumulation of advanced glycation end products and the molecules of the molecular pattern associated with damage also represent important mechanisms that mediate inflammation of the diabetic heart, mainly by acting on Toll-like receptors. A high expression of mediators of inflammation of the diabetic heart directly promotes cardiac disorders through the modulation of multiple mechanisms. In fact, it is known that intracellular signaling pathways in the heart are modulated that promote hypertrophy of cardiomyocytes, death, fibrosis and heart failure.
The understanding of the pathophysiology and pathogenesis in patients with diabetic cardiomyopathy has provided better management options. This includes, lifestyle modifications, improved diabetic control, the management of coexisting hypertension and coronary artery disease if present, lipid-lowering therapies and the management of heart failure.