P 202 - Role of Redox Signaling in cardioinflammation and chronic heart failure

Abstract

Disruptions in the physiologic maintenance of the redox potential in cardiomyocytes with several biological processes, ultimately leading to cell death. A progressive rise of oxidative stress due to altered reduction–oxidation (redox) homeostasis appears to be one of the hallmarks of the processes that regulate gene transcription in cardiac hypertrophy and heart failure development. Reactive metabolites and NAD particularly, serve as signaling messengers for the evolution and perpetuation of the inflammatory process that is often associated with cell death, degeneration, alteration transcription factors in many human disease states and inflammatory-related injury. These proinflammatory factors act as potent stimuli in cardiac inflammation through upregulation of diverse inflammatory genes, including matrix metalloproteinases (MMPs), cytosolic phospholipase A2 (cPLA2), cyclooxygenase-2 (COX-2), and adhesion molecules. In this review, we discuss the mechanisms underlying the intracellular signaling pathways, especially ROS, involved in the expression of several inflammatory proteins induced by proinflammatory factors in cardiomyocytes. The present review elaborates on the role of the redox-sensitive and oxygen-sensitive transcription factor NF-κB and tumor necrosis factor alpha in mediating cardiac hypertrophy and chronic heart failure.