Oxidative Stress in Vascular Pathophysiology

Dear Colleagues,

In the physiological context, reactive oxygen species (ROS) play a fundamental role in controlling vascular and heart functions through the modulation of several redox-sensitive signaling pathways. However, the excess of ROS production inevitably leads to oxidative stress (OS), a condition characterized by an imbalance between pro-oxidant species and antioxidant systems, potent ROS-detoxifying enzymes employed by vascular cells and cardiomyocytes to preserve their integrity against OS-dependent damages, thus ensuring the normal cardiovascular function. The development of a pro-oxidant phenotype triggers cellular and molecular mechanisms driving inflammation, endothelial dysfunction, and the associated myocardial infarction and other cardiovascular diseases. Although the role of OS in the onset and progression of atherosclerosis and its late thrombotic complications is unquestionable, and although several antioxidants have been found to induce cardioprotection in preclinical models, these agents have shown disappointing results in large-scale randomized controlled trials. Hence, the identification and development of new therapies are urgently required to mitigate the cardiovascular burden and reduce associated risk factors, ameliorating the quality of life and patient health status. In this context, the present topic addresses the latest findings aiming to highlight novel mechanisms whereby physiological ROS levels modulate cardiovascular functions, identify novel molecular actors and pharmacological agents that could prevent vascular and cardiac OS, and improve vasculature function for translating novel cardioprotective therapies and biomarkers into the clinical scenario for patient benefit.

Prof. Dr. Claudia Penna
Prof. Dr. Tommaso Angelone
Dr. Roberto Berra-Romani
Dr. Francesco Lodola
Dr. Francesco Moccia
Dr. Carmine Rocca
Topic Editors