The Diabetes Mellitus–Atherosclerosis Connection: The Role o
Diabetes mellitus comprises a group of carbohydrate metabolism disorders that share a common main feature of chronic hyperglycemia that results from defects of insulin secretion, insulin action, or both. This review summarizes the main aspects of diabetes mellitus that possibly affect the atherogenic process and its relationship with chronic inflammation.

Atherosclerosis is a widespread chronic inflammatory disorder of the arterial wall that often leads to disability and even death. At its final stages, atherosclerosis manifests itself as a lesion of the intimal layer of the arterial wall and accumulation of plaques. Subsequent erosion or rupture of atherosclerotic plaques triggers thrombotic events that can potentially be fatal.

Decades of intensive research made it clear that atherosclerosis has complex pathogenesis, the main components of which are lipid accumulation and chronic inflammation in the arterial wall. Atherosclerosis is classically associated with altered lipid metabolism and hypercholesterolemia. An elevated level of circulating modified low-density lipoprotein (LDL) is a known risk factor of cardiovascular diseases. However, the disease pathogenesis appears to be more complex than lipid metabolism changes and involves multiple factors, the most prominent of which is inflammation.

Both types of diabetes mellitus have been shown to be independent risk factors for accelerated atherosclerosis development. It is now clear that the pathogenesis of diabetes mellitus and atherosclerosis are closely linked, but the mechanisms and molecular interactions of this linkage are still under discussion. Among the known pathological mechanisms connecting diabetes and atherosclerosis are dyslipidemia, hyperglycemia with AGE production, increased oxidative stress, and inflammation.

Despite the continuing search for novel therapeutic approaches, few medications have shown strong beneficial effects with regard to reducing the risk of atherosclerosis development in the specific population of diabetic patients. Adequate glycemic control and reduction of known risk factors remain the most frequently used strategies for protecting such patients. More studies are needed to reveal the exact signaling mechanisms of diabetes-associated macrovascular damage and to identify specific therapeutic targets.