Endothelial cells are key modulators of multiple physiological processes, and their impairment may result inthe generation of endothelial dysfunction and ultimately cardiovascular diseases. Under physiologic conditions, reactiveoxygen and nitrogen mediators of endothelial cells act to propagate signals driven by different stimuli, by forming moleculeswith a longer half-life like hydrogen peroxide. Reactive oxygen species (ROS) are constantly produced as a consequenceof aerobic metabolism. Under physiologic conditions, their tendency to cause oxidative damage is counterbalancedby the action of antioxidants or oxidant-scavenging enzymes. An imbalance in favour of oxidants leads to oxidativestress, which can result in cardiomyocyte apoptosis and reduced bioavailability of vascular nitric oxide (NO). Together,these processes may lead to altered vasodilatation of the coronary, pulmonary and peripheral vascular beds. Myeloperoxidaseis a key enzyme, capable of impairing intracellular NO reservoirs as well as producing oxidized amino acids such as3-chlorotyrosine or 3-nitrotyrosine. Recent literature data have shown that apart neutrophils, this enzyme may be expressedby other cell types, and remarkably by endothelial cells both in vitro and in vivo, as a consequence of the exposureto oxidative stress. In this review we analyze recent literature and patents related to the detection, quantification and roleof myeloperoxidase as a biomarker in patients affected by chronic heart failure or other cardiovascular diseases. A particularfocus is given to analytical approaches aimed to detect early signals of variations in ROS or related enzymes or theirby-products, via serological or other low-invasivity assays. The developments in this field may constitute a key improvementof the ability to manage and treat patients suffering from CHF as well as allowing to elucidate the molecular mechanismsbehind the clinical phenomena.
- Molecular Medicine
- Clinical Biochemistry