Dear Colleagues,

Oxidative stress is a phenomenon caused by an imbalance between production and accumulation of reactive oxygen species (ROS) in cells and tissues and the ability of a biological system to detoxify these reactive products. Evidence from experimental and clinical studies has shown that oxidative/nitrosative stress and inflammation associated with metabolic disorders such as obesity, hypertension, and diabetes are conducive to fibrosis, diastolic dysfunction, heart failure, and ischemia/reperfusion damage. Numerous studies have evaluated the primary contribution of oxidative stress to the pathogenesis of atherosclerotic disease.The effect of free radicals at the endothelial level is relevant and associated with increased expression of molecules of vascular adhesion (Vcam-1), oxidation of low-density lipoprotein (LDL), and proliferation of vascular smooth muscle cells. In this context, factors related to lifestyle, such as eating habits, can play a crucial role in the pathogenesis of oxidative stress, which can cause an increase in physiological ROS production that lowers the effectiveness of antioxidant defenses. In particular, it has been shown that an increase in caloric intake and/or the ingestion of oxidized by-products contained in inadequately controlled foods can increase the physiological "load" of oxidizing agents, while a reduced intake and/or decreased bioavailability of natural antioxidants—usually abundantly distributed in fruit and vegetables—can compromise the body's ability to eliminate ROS.

For this Special Issue of Cells, I solicit your contribution in the form of an original article or review on the various molecular networks that oxidative stress and nutrition can modify, leading to endothelial alterations and cardiovascular damage.

Prof. Lorenza Speranza
Guest Editor

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• Oxidative stress
• Nitrosative stress
• Cardiovascular disease
• Nutrition