Semin Thromb Hemost 2013; 39(05): 477-488
DOI: 10.1055/s-0033-1343888
Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.

Prothrombotic Changes in Diabetes Mellitus

Olivier Morel
1   Unité de recherche EA 7293 Stress vasculaire et tissulaire en Transplantation, Faculté de Médecine, Université de Strasbourg, Strasbourg, France
2   Pôle d'activité médico-chirurgicale, Cardio-Vasculaire des Hôpitaux, Universitaires de Strasbourg, Strasbourg, France
,
Laurence Jesel
1   Unité de recherche EA 7293 Stress vasculaire et tissulaire en Transplantation, Faculté de Médecine, Université de Strasbourg, Strasbourg, France
2   Pôle d'activité médico-chirurgicale, Cardio-Vasculaire des Hôpitaux, Universitaires de Strasbourg, Strasbourg, France
,
Malak Abbas
3   Plateforme de Recherche et d'Analyses en Sciences de l'Environnement, Ecole Doctorale des Sciences et Technologies, Université Libanaise, Hadath, Beirut, Lebanon, Beyruth, Lebanon
,
Nicolas Morel
4   Pôle d'Urgences, CHU Bordeaux, Bordeaux, France
› Institutsangaben
Weitere Informationen

Publikationsverlauf

Publikationsdatum:
29. April 2013 (online)

Zoom Image

Abstract

Although our understanding of vascular pathology has greatly improved in recent years, the cellular and molecular mechanisms underlying the enhanced thrombotic propensity in type 2 diabetes mellitus (T2DM) remain incompletely characterized. Detrimental interactions between activated vascular cells (i.e., platelets, leukocytes, endothelial cells) and the vulnerable atheromatous plaque are a major determinant of the increased atherothrombotic burden in T2DM patients. Endothelial damage and accelerated senescence, impairment of the endothelial progenitor cell repair system, plaque neovascularization and inflammation, decreased clearance of detrimental molecules within the plaque, and increased expression of matrix metalloproteinases may collectively contribute to intraplaque hemorrhage and subsequent rupture. Notably, recent data demonstrates the central importance of the tissue factor-microparticle–mediated pathway in diabetic thrombophilia and cardiovascular complications. Acting as detrimental amplifiers of various biological responses (including thrombogenicity and plaque remodeling), microparticles have also emerged as a key marker of global vascular damage in T2DM patients. Available evidence suggests that targeting the tissue factor-microparticle pathway may be a promising approach for reducing the burden of the atherosclerotic complications of diabetes.