Role of the interaction between endoplasmic reticulum and mitochondria in human microparticles induced endothelial dysfunction.
Metabolic syndrome (MetS) consists of a constellation of metabolic abnormalities such as central obesity, impaired fasting glucose, hypertriglyceridemia, low HDL cholesterol and hypertension. Cardiovascular diseases are the primary clinical outcome of MetS whereas endothelial dysfunction represents a primary disturbance in cardiovascular events. Recently, it has been shown that microparticles (MPs), small membrane vesicles released from the plasma membrane of activated and/or apoptotic cells, are involved in the pathogenesis of MetS by inducing endothelial dysfunction through the decrease of nitric oxide (NO) production. Also, MPs from apoptotic T cells induce endothelial dysfunction by decreasing NO production. However, the mechanism through which this endothelial dysfunction takes place is not completely elucidated. Thus, the objective of this study is to study the mechanisms through which human MPs induce endothelial dysfunction.
During Beirut Antioxidants World Congress, Dr. Kazem Zebara from Lebanese University , will present about "Role of the interaction between endoplasmic reticulum and mitochondria in human microparticles induced endothelial dysfunction".
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