Open Access
Article
Role of endothelial cell stress in the pathogenesis of chronic heart failure
Rita Anzalone1,Giampiero La Rocca1,Antonino Di Stefano1,Francesca Magno1,Simona Corrao1,Marco Carbone1,Tiziana Loria1,Melania Lo Iacono1,Ermanno Eleuteri1,Marilena Colombo1,Francesco Cappello1,Felicia Farina1,Giovanni Zummo1,Pantaleo Giannuzzi1
1
Human Anatomy Section, Department of Experimental Medicine, University of Palermo, Via del Vespro 129, 90127 Palermo, Italy
DOI: 10.2741/3376 Volume 14 Issue 6, pp.2238-2247
Published: 01 January 2009
(This article belongs to the Special Issue Progresses in heart failure diagnosis and treatment)
Abstract

Endothelial cells are key modulators of diverse physiological processes, and their impaired function is a cause of numerous cardiovascular diseases. Under physiologic condition, the reactive oxygen and nitrogen mediators in endothelia lead to the signal propagation of the initial stimulus, by forming molecules with a longer half-life like hydrogen peroxide. Hydrogen peroxide is the focus of growing attention in endothelial biology, and consequently the enzymes involved in its generation and clearance are viewed as novel mediators of great importance. In particular, among peroxidases, myeloperoxidase is recognized as a key enzyme, capable of impairing intracellular NO reservoirs as well as producing oxidized amino acids such as 3-chlorotyrosine or 3-nitrotyrosine. This process switches the functional pathways from normal signalling to a condition characterized by oxidative and/or nitrosative stress. Understanding the molecular mechanisms involved in these stress responses in endothelium will lead to better therapeutic strategies for oxidative stress-driven cardiovascular diseases.

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Rita Anzalone, Giampiero La Rocca, Antonino Di Stefano, Francesca Magno, Simona Corrao, Marco Carbone, Tiziana Loria, Melania Lo Iacono, Ermanno Eleuteri, Marilena Colombo, Francesco Cappello, Felicia Farina, Giovanni Zummo, Pantaleo Giannuzzi. Role of endothelial cell stress in the pathogenesis of chronic heart failure. Frontiers in Bioscience-Landmark. 2009. 14(6); 2238-2247.