Ricerc@Sapienza

The pathogenic mechanism underlying ischemic stroke involves the embolization of a complicated and unstable carotid plaque. This abrupt clinical presentation is the strongest signal of discontinuity in the natural history of atherothrombosis. It is widely known that the long-established cardiovascular risk factors contribute to atherosclerosis by inducing endothelial dysfunction and intra-parietal inflammation. However, the diverse mechanisms involved in triggering the acute inflammatory process and the specific factors that contribute to plaque instability remain poorly understood.
The accumulation of reactive oxygen species (ROS) and the subsequent triggering of the inflammation response are involved in the cardiovascular functional and structural damage, giving ROS a solid pathogenic role underlying all major cardiovascular diseases. The relevance of monitoring oxidative stress in cardio-cerebro-vascular diseases is underscored by several experimental data and the link between mitochondrial dysfunction and ROS production, studying circulating peripheral blood mononuclear cells (PBMCs), has been explored. PBMCs circulate in the blood stream and can directly distribute and amplify oxidative stress in the cardiovascular system; for this reason, they might reflect quite closely the cardiovascular oxidative stress condition and so they might be useful to understand the mechanisms involved in the pathogenesis of vascular diseases.
Based on that, we will verify whether the analysis of PBMCs may represent a non-invasive tool (i) to detect a possible status of oxidative stress related to Carotid Atherosclerotic Disease (ii) to verify the potential involvement of mitochondrial dysfunction as a contributory pathogenic mechanism in the progression of carotid plaque, (iii) to screen patients with vulnerable/symptomatic carotid plaque.