Oxidative Stress in Cardiovascular Diseases and Vascular Pathophysiology

Dear Colleagues,

Reactive oxygen species (ROS), particularly superoxide anion and hydrogen peroxide, play an essential role in numerous cellular physiological processes by modulating several signaling pathways. In contrast, the overproduction of ROS and/or the impairment of endogenous antioxidant defenses induces an imbalance that ultimately leads to a situation of oxidative stress that is implicated in vascular and metabolic diseases, including hypertension, atherosclerosis and diabetes; these constitute the main risk factors for stroke, myocardial infarction and heart failure. Among other effects, oxidative stress alters gene expression, causes endothelial dysfunction, promotes the remodeling of the extracellular matrix, and exacerbates inflammatory and senescent vascular processes. Vascular oxidant-generating enzymes include NADPH oxidases, xanthine oxidases, lipoxygenases, mitochondrial oxidases, and nitric oxide synthases. We still do not fully understand the underlying mechanisms of oxidative stress and the pathological effects that an increase in ROS production has in cardiovascular tissue. Unravelling these underlying causes is essential to enhancing disease therapy. This Special Issue will focus on the novel mechanisms of oxidative stress, its impact on vascular inflammation and dysfunction, the identification of principal ROS-generating enzymes, with a special focus on the NADPH oxidase family and mitochondria, and the potential benefit of targeting these specific sources of oxidative stress to improve vascular function. We invite you to submit your latest research findings or a review article to this Special Issue.

Prof. Dr. Guillermo Zalba
Guest Editor

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• atherosclerosis
• diabetes
• heart failure
• inflammation
• myocardial infarction
• NADPH oxidase
• oxidative stress
• reactive oxygen species
• stroke