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

Paneni, Francesco ; Beckman, Joshua A. ; Creager, Mark A. ; Cosentino, Francesco

In: European Heart Journal, 2013, vol. 34, no. 31, p. 2436-2443

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    Titre
    • Diabetes and vascular disease: pathophysiology, clinical consequences, and medical therapy: part I
    Auteur
    • Paneni, Francesco. Cardiology and Cardiovascular Research, University of Zürich, Zürich, Switzerland
    • Beckman, Joshua A.. Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA
    • Creager, Mark A.. Cardiovascular Division, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA
    • Cosentino, Francesco. Cardiology and Cardiovascular Research, University of Zürich, Zürich, Switzerland
    Type de document
    • Postprint
    Langue
    • Anglais
    Publié dans
    • European Heart Journal, 2013, vol. 34, no. 31, p. 2436-2443. Oxford University Press
    Autre version électronique
    Identifiant OAI-PMH
    • oai:doc.rero.ch:297866
    Summary
    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