Oxidative Stress and Reactive Oxygen Species in Cardiovascular Disease

Dear Colleagues,

Cardiovascular disease (CVD) is the leading cause of mortality and the most expensive health condition worldwide. Pre-clinical and clinical studies associated the imbalance of oxidative stress and antioxidant status with the pathogenesis of CVD. Thus, upregulation of reactive oxygen species (ROS)-producing enzymes such as NADPH oxidase, along with downregulation of antioxidant enzymes, such as superoxide dismutase and glutathione peroxidase, occurs during CVD development. This imbalance may predispose to athero-thrombosis by enhancing platelet and clotting activation and inducing endothelial dysfunction.

Recently, gut-derived products, such as trimethylamine N-oxide (TMAO) and lipopolysaccharide (LPS), are emerging as novel cardiovascular risk factors. In particular, LPS is a pro-atherogenic molecule through its pro-oxidant properties, which are mediated by NOX2 activation, one of the most important cellular producers of ROS. LPS may translocate into systemic circulation upon microbiota dysbiosis-induced gut barrier dysfunction and can amplify platelet responses via Toll-like receptor 4 (TLR4) activation and NOX2-derived ROS formation. Another mechanism involved in maintaining redox balance is autophagy which is a crucial adaptive cellular response to oxidative stress, removing excessive cellular ROS; in fact, recent evidence showed that oxidative stress Nox2-mediated is associated with autophagy inhibition. Furthermore, autophagy preserves endothelial function through attenuation of ROS production and inflammatory signaling and increasing nitric oxide (NO) bioavailability.

Reducing oxidative stress represents a promising approach to the prevention and treatment of CVD. Therefore, the identification of strategies targeted to modulate redox balance, by activation or inhibition of specific enzymatic sources of ROS, improvement of gut microbiota and permeability, or potentiating pro-autophagic effects, is necessary.

This Special Issue will focus on the causes and consequences of oxidative stress in CVD exploring cellular and molecular mechanisms involved and emerging treatment strategies.

Dr. Roberto Carnevale
Dr. Vittoria Cammisotto
Guest Editors

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• oxidative stress, reactive oxygen species
• cardiovascular disease, cardiovascular risk factor
• oxidative stress biomarkers, redox signaling
• platelet activation and oxidative stress
• endothelial dysfunction and oxidative stress
• dysbiosis and oxidative stress
• autophagy and oxidative stress
• antioxidant therapy