Figure 1.

Oxidative stress occurs when the production of reactive oxygen species (ROS) exceeds the antioxidant defense. Obesity leads to the increased systemic oxidative stress. In adipose tissue, ROS can be generated by NADPH oxidase, xanthine oxidase, and mitochondrial oxidative phosphorylation system. On one hand, the production of ROS in adipose tissue of obese subjects leads to insulin resistance, dysregulated adipokines secretion, inflammation and increased protein carbonylation. On the other hand, ROS in adipose tissue could promote adipocyte differentiation and thermogenesis in brown adipose tissue (BAT). A variety of enzymes, including superoxide dismutase (SOD), catalase, glutathione peroxidases (GPx), heme oxygenase (HO), and peroxiredoxins (Prxs), can reduce ROS burden and act as antioxidant defense in adipose tissue. Adipose tissue exerts direct effects on vascular system through releasing a wide range of bioactive products, which include circulating adipokines. Perivascular adipose tissue (PVAT) is important adipose tissue that regulates vascular function and remodeling due to its close proximity. In PVAT, the modulation of vascular contractility is conducted through the secretion of PVAT-derived relaxing factors (PVRFs) and PVAT-derived contracting factors (PVCFs). In obesity, increased oxidative stress, inflammation and eNOS dysfunction in PVAT may alter the balance between PVRFs and PVCFs. Obesity-induced PVAT dysfunction leads to the reduction of PVRFs and the production of PVCFs, hence causing enhanced vasocontraction. In addition, chronic changes in the adipokines profile may result in the pathological vascular remodeling which can further increase the risk of CVDs.