Institute of Cardiology, G. d'Annunzio University, Chieti, Italy.
Vascul Pharmacol. 2011 Mar-Jun;54(3-6):75-9. doi: 10.1016/j.vph.2011.03.007. Epub 2011 Mar 29.
Although the mechanisms by which insulin-resistance and hyperglycemia lead to cardiovascular disease are still incompletely understood, all mechanisms apparently converge on the vessel wall and the endothelium as a common disease target. Endothelial cells play a crucial role in vascular homeostasis, providing a functional barrier and modulating several signals involved in vasomotion, as well as antiplatelet, anti-inflammatory, anti-proliferative, and anti-oxidant properties of the vessel wall. Endothelial cell dysfunction occurs early in diabetes and insulin resistance states. Since atherosclerosis may result from an imbalance between the magnitude of vascular injury and the capacity of repair, a role has been recently postulated for a defective mobilization of vascular progenitors, including endothelial progenitor cells, in the pathogenesis of vascular disease. Here we summarize the evidence for such an occurrence. We also here highlight how new insights into pathways of vascular damage in diabetes may indicate new targets for preventive and treatment strategies.
尽管胰岛素抵抗和高血糖导致心血管疾病的确切机制仍不完全清楚，但所有机制显然都集中在血管壁和内皮作为共同的疾病靶点。内皮细胞在血管稳态中发挥着至关重要的作用，提供了一个功能性屏障，并调节血管舒缩、抗血小板、抗炎、抗增殖和抗氧化等多种信号。内皮细胞功能障碍在糖尿病和胰岛素抵抗状态早期就已经发生。由于动脉粥样硬化可能是由于血管损伤的程度和修复能力之间的失衡所致，最近有人提出，包括内皮祖细胞在内的血管祖细胞的动员缺陷在血管疾病的发病机制中起作用。在这里，我们总结了这方面的证据。我们还在这里强调了糖尿病中血管损伤途径的新见解如何为预防和治疗策略提供新的靶点。
