Dear Colleagues,

In the last three decades, advances in research and therapeutics have signicantly reduced the morbidity and mortality associated with cardiovascular-related diseases. However, as obesity and metabolic syndrome are rapidly becoming a world-wide epidemic, the incidence of cardiovascular disase is on the rise and there is a critical need for new molecular targets that take into account these co-morbidities. Reactive oxygen species (ROS) production is an integral part of both normal cardiometabolic homeostasis and cardiometabolic pathologies. The dual role of ROS is underscored by the failure of antioxidant therapies to provide clear cardiometabolic benefits. Furthermore, the adaptive responses of the vasculature to exercise, which protect from cardiometabolic diseases, are dependent on ROS signaling. Indeed, recent studies have demonstrated that ROS are necessary for the regulation of a myriad of normal cellular redox processes, including intracellular signaling, metabolic homeostasis, and transcriptional regulation. In terms of pathology, most cardiometabolic diseases demonstrate signatures of ROS damage and chronic inflammation. ROS are both mediators of pro-inflammatory signaling and the product of inflammation, and likely contribute to a toxic milieu that furthers tissue damage in disease states. In fact, a recent clinical trial demonstrated the effectiveness of targeting inflammation by reducing injury during major cardiovascular events. Therefore, understanding the intersection between inflammation, reactive oxygen species, metabolism, and exercise adaptation in physiologic and pathologic settings is essential to a better understanding of cardiometabolic health, disease, and thereapeutic strategies.

The goal of this special issue is to assemble a collection of state-of-the-art research and review articles describing:

1. Mechanisms of ROS regulation including timing, location, and sources of obesity (e.g., NADPH oxidases, nitric oxide synthase, lipoxygenases, mitochondria), and inflammation and metabolic syndrome in the context of cardiovascular disease.
2. Pharmacologic and non-pharmacologic strategies of manipulating localized redox-signaling pathways to prevent cardiovascular consequences, including inflammation and dysregulation of cardiovascular metabolism.
3. Redox mechanisms by which diet and/or exercise modify inflammation and the effects of cardiovascular diseases and cardiometabolic syndrome.

Prof. Dr. Francis J. Miller, Jr.
Dr. Siobhan M. Craige
Guest Editors

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• Redox signaling: oxidative stress, reactive oxygen species, NADPH oxidase, mitochondria, antioxidants
• Inflammation: cytokines, chemokines, inflammatory signaling
• Cardiometabolic diseases: diabetes, obesity, metabolism, metabolic disease
• Exercise: exercise adaptation, cardiometabolic preconditioning, exercise to prevent disease
• Heart disease: myocardial infarction, ischemia/reperfusion, cardiometabolic dysfunction
• Vascular disease: atherosclerosis, hypertension, restenosis, stroke, neointima, thrombosis, peripheral artery disease, aneurysm, vasculitis