Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I

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ID: 294921
2013
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Abstract
Hyperglycemia and insulin resistance are key players in the development of atherosclerosis and its complications. A large body of evidence suggest that metabolic abnormalities cause overproduction of reactive oxygen species (ROS). In turn, ROS, via endothelial dysfunction and inflammation, play a major role in precipitating diabetic vascular disease. A better understanding of ROS-generating pathways may provide the basis to develop novel therapeutic strategies against vascular complications in this setting. Part I of this review will focus on the most current advances in the pathophysiological mechanisms of vascular disease: (i) emerging role of endothelium in obesity-induced insulin resistance; (ii) hyperglycemia-dependent microRNAs deregulation and impairment of vascular repair capacities; (iii) alterations of coagulation, platelet reactivity, and microparticle release; (iv) epigenetic-driven transcription of ROS-generating and proinflammatory genes. Taken together these novel insights point to the development of mechanism-based therapeutic strategies as a promising option to prevent cardiovascular complications in diabetes.
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openalex_W2158106881 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Francesco Paneni, Joshua A. Beckman, Mark A. Creager, Francesco Cosentino
Journal european heart journal
Year 2013
DOI
10.1093/eurheartj/eht149
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