Key result
Perivascular adipose tissue-derived ROS emerge as a key driver of vascular injury in cardiometabolic disease.
Why the study?
Dysfunctional perivascular adipose tissue (PVAT) generating reactive oxygen species (ROS) is suggested to link cardiometabolic risk factors to vascular dysfunction, but its pathophysiological role requires summarization.
Dysfunctional perivascular adipose tissue generates reactive oxygen species that may contribute to vascular injury in cardiometabolic diseases.
May identify novel vascular target in cardiometabolic disease; leaves open need for prospective studies to confirm causality and therapeutic relevance.
Most of the systemic blood vessels are surrounded by the perivascular adipose tissue (PVAT). Healthy PVAT is anticontractile and anti-inflammatory, but a dysfunctional PVAT has been suggested to link cardiometabolic risk factors to vascular dysfunction. Vascular oxidative stress is an important pathophysiological event in cardiometabolic complications of obesity, type 2 diabetes, and hypertension. PVAT-derived adipocytes generate reactive oxygen species (ROS) including superoxide anion and hydrogen peroxide that might signal to the vascular wall. Therefore, an abnormal generation of ROS by PVAT emerges as a potential pathophysiological mechanism underlying vascular injury. This review summarizes new findings describing ROS production in the PVAT of several vascular beds, major sources of ROS in this tissue including mitochondria, NADPH oxidase and eNOS uncoupled, and finally, changes in ROS production affecting vascular function in the presence of cardiometabolic risk factors and diseases.
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Victorio et al. (2019) conducted a review in Cardiometabolic diseases. Perivascular adipose tissue oxidative stress was evaluated. Perivascular adipose tissue-derived reactive oxygen species emerge as a potential pathophysiological mechanism underlying vascular injury in cardiometabolic diseases.
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