Dear Colleagues,

Reactive oxygen species (ROS) overproduction and oxidative stress have consistently been involved in the pathogenesis of the cardiovascular complications associated with metabolic disorders such as insulin resistance, obesity and dyslipidemias. Oxidative stress also seems to be the link between inflammation and cardiovascular impairment in metabolic diseases. Mitochondria, NADPH oxidases, uncoupled NO synthase and lipoxygenases are major accepted sources of ROS overproduction, which along with impaired antioxidant defenses lead to oxidative stress in cardiac and vascular tissues in insulin-resistant states. Mitochondria render most of the basally produced endogenous superoxide in cells, and an excess of mitochondrial superoxide derived from increased electron transport chain activity has traditionally been proposed as a major cause as of non-insulin-dependent diabetic complications. However, recent evidence suggests that metabolic impairment is associated with reduced mitochondrial ROS production in diabetes and obesity linked to altered activity of the energy sensor AMPK. On the other hand, activation of the endoplasmic reticulum (ER) stress response is also involved in the pathogenesis of metabolic disorders, and cross-talk between ER and mitochondria contributes to oxidative stress underlying endothelial and vascular dysfunction. Metabolic impairment reduces the activity of antioxidant systems such as nuclear factor erythroid 2-like 2 (Nrf2) and activates the redox-sensitive transcription factor NFκB signaling pathway that regulates the expression of inflammatory genes in cardiomyocytes as well as endothelial and vascular smooth muscle cells, thus leading to low-grade chronic inflammation associated with endothelial dysfunction and the development of atherosclerotic cardiovascular disease.

The aim of this Special Issue is to further elucidate the specific mechanisms and signaling pathways interrelating oxidative stress and inflammation in the pathogenesis of insulin-resistance-associated cardiovascular complications.

Prof. Dr. Dolores Prieto
Prof. Dr. Maria Carmen Martínez
Guest Editors

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• metabolic disease
• insulin resistance
• mitochondria
• ER stress
• inflammation
• cardiovascular disease