The condition is vascular injury the underlying cause can be due to a metabolic syndrome, insulin resistance, prediabetes, and overt type 2 diabetes mellitus are associated with an accelerated atherosclerosis (atheroscleropathy).
The common (spontaneous atherosclerosis) pathophysiologic mechanisms, namely, endothelial injury with early platelet involvement and subsequent progressive smooth muscle cell proliferation and thrombosis leading to vascular occlusion. Understanding the mechanisms of this process has made it possible to include strategies to limit vascular injury and reduce subsequent thrombotic and proliferating cellular responses.
In contrast to spontaneous atherosclerosis, a more significant denuding endothelial injury appears to be the critical initiating event, followed by intense platelet involvement and thrombus formation, leading to an initial predominant process of smooth muscle cell proliferation in accelerated atherosclerosis. Risk factors like cigarette smoking and hypertension play an important role in this process.
Atherosclerosis (Atherosclerosis, AS) is a form of vascular endothelial cells (vascular endothelial cell, VEC) damage, vascular smooth muscle cells (vascular smooth muscle cell, VSMC) proliferation as the main pathological features of vascular disease. Endothelial cells (endothelial cell, EC) dysfunction and injury is the initiating AS part of the formation of oxidized low density lipoprotein (oxidized low density lipoprotein, ox-LDL) is recognized as the risk of damage caused by EC one of the factors The VEC produced in addition to direct oxidative damage, promote mononuclear cells (monocyte, MC) and the VEC adhesion to EC dysfunction occurred while AS is active as an important step took place, but also through the signal transduction system, leading to cell production oxidative stress in the formation of AS plays a key role.
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