Tracing the proteomic fingerprint of the diabetic aorta?

Abstract

Diabetes mellitus is a worldwide epidemic, and the percentage of the US population diagnosed with diabetes mellitus between 1980 and 2010 increased from 2.5% to 6.9%.1 Nearly 27% of people >65 years of age have diabetes mellitus. If current trends continue, 1 in 3 US adults will experience diabetes mellitus by 2050. This can be attributed to lifestyle choices contributing to obesity.2 One of the main causes of death and disability in patients with diabetes mellitus are vascular complications, affecting both the macro- and the microvasculature.3 Macrovascular manifestations include atherosclerosis leading to coronary artery disease, peripheral arterial disease, and stroke. Microvascular changes, on the other hand, encompass diabetic nephropathy, retinopathy, and neuropathy. Article see p 161 Although there is compelling evidence for the association of diabetes mellitus and vascular disease, the underlying pathophysiological mechanisms remain to be elucidated. Advanced glycation end products, as well as reactive oxygen species, are suggested to be 2 of the major culprits leading to vascular damage.4,5 Extracellular matrix proteins can become glycated by nonenzymatic reactions of sugar moieties, which alter protein function in target tissues.6 Major histological changes are apparent in diabetic vessels, including increased intima–media thickness and excessive extracellular matrix deposition.5 Yet, despite many patients with diabetes mellitus following a tight glycemic control regime, they are still experiencing vascular complications. Notably, …