Atherosclerosis, a multifactorial disease of the large arteries, is the major cause of heart disease and stroke worldwide. Epidemiological studies have discovered several relevant environmental and genetic risk factors associated with this pathology. Genomic and proteomic-based strategies in humans and rodent models have been instrumental in discovering genes and proteins involved in the initiation and progression of atherosclerosis. Moreover multiple genome-wide approaches are underway to identify variants in the human genome that predispose to, or protect from, cardiovascular disease. Our views of the pathophysiology of atherosclerosis have evolved substantively over the past century and now it is recognized that inflammation and angiogenesis are important features in atherosclerotic plaque development and destabilization. The clinical complications of atherosclerosis are caused by thrombus formation, which in turn results from rupture of an unstable atherosclerotic plaque. © 2010 Springer Science+Business Media B.V.
A3 Adenosine receptors, HIF-1 modulation and atherosclerosis
GESSI, Stefania;BOREA, Pier Andrea
2010
Abstract
Atherosclerosis, a multifactorial disease of the large arteries, is the major cause of heart disease and stroke worldwide. Epidemiological studies have discovered several relevant environmental and genetic risk factors associated with this pathology. Genomic and proteomic-based strategies in humans and rodent models have been instrumental in discovering genes and proteins involved in the initiation and progression of atherosclerosis. Moreover multiple genome-wide approaches are underway to identify variants in the human genome that predispose to, or protect from, cardiovascular disease. Our views of the pathophysiology of atherosclerosis have evolved substantively over the past century and now it is recognized that inflammation and angiogenesis are important features in atherosclerotic plaque development and destabilization. The clinical complications of atherosclerosis are caused by thrombus formation, which in turn results from rupture of an unstable atherosclerotic plaque. © 2010 Springer Science+Business Media B.V.I documenti in SFERA sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.