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

By F. Paneni, Joshua A. Beckman, M. Creager, F. Cosentino. European Heart Journal, 2013

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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.

Subfields: Cardiology and Cardiovascular Medicine, Epidemiology, Immunology

View Paper: https://www.semanticscholar.org/paper/a14b57c890bd41070768b107205d14645f55fcea

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Citations in the corpus

2018 ESC/EACTS Guidelines on myocardial revascularization. (2019, neutral): “In one prospective registry including 4616 patients with multivessel disease and severe HFrEF, propensity score-matched comparison revealed similar survival (mean follow-up 2.9 years) with PCI (using EES) vs. CABG.250 PCI was associated with a higher risk of MI, particularly in patients with incompl”
Endothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing (2012, background): “Hyperglycemia results in BH4 deficiency and eNOS dysfunction characterized by a decrease in NO with a concomitant increase in superoxide production [111, 142, 143].”
Diabetes mellitus, fasting blood glucose concentration, and risk of vascular disease: a collaborative meta-analysis of 102 prospective studies (2011, neutral): “…subtypes (fatal or non-fatal ischaemic, haemorrhagic, or unclassiﬁ ed stroke); and deaths attributed to the aggregate of other vascular disorders (consisting of heart failure, cardiac dysrrhythmia, sudden death, hypertensive disease, pulmonary embolism, and aortic aneurysm; webappendix p 21).”