Glucose-induced vascular smooth muscle dysfunction: the role of protein kinase C.
Glucose-induced vascular smooth muscle dysfunction: the role of protein kinase C.
复制标题
葡萄糖引起的血管平滑肌功能障碍：蛋白激酶 C 的作用。
DOI：
10.1097/00004872-199505000-00001
复制
发表时间：
1995
影响因子：
4.9
通讯作者：
Williams,B
中科院分区：
文献类型：
--
作者：
Williams,B
糖尿病的特征是微血管和大血管疾病的过早发展[1]。人们普遍认为，高血压的共存极大地加速了糖尿病患者血管病变的发展。此外，糖尿病患者比非糖尿病人群更容易患高血压。因此，评估糖尿病患者血管损伤的发生机制与了解相当一部分高血压患者的心血管疾病的发病机制有关。以前的[2]和MORC最近的[3]临床试验都强调高血糖是心血管疾病发展的独立危险因素。当细胞外葡萄糖浓度升高时，血管细胞摄取葡萄糖在很大程度上是不依赖于胰岛素的，这使得血管细胞容易受到葡萄糖诱导的损伤。尽管已经探索了许多可能性，包括葡萄糖诱导的细胞内山梨醇积累增加[4]，晚期糖基化终产物的形成[5]，以及更直接的葡萄糖诱导的细胞氧化还原状态的改变[6]，但高的细胞外-细胞内葡萄糖流量促进血管损伤的发病机制尚未得到证实。人们还关注蛋白激酶C在糖尿病诱导的血管损伤中的潜在作用||7-14]。在这一点上，蛋白激酶C是一个有吸引力的候选者，因为它在调节不同类型细胞内的许多生物学功能中发挥着关键作用[15-17]。此外，血管通畅
Diabetes mellitus is characterized by the premature development of microvascular and macrovascular disease [1]. It is widely accepted that the development of vas-cular disease in diabetic patients is greatly accelerated by the coexistence of hypertension. Moreover, patients with diabetes are more commonly hypertensive than the non-diabetic population. For these reasons evaluating the mechanisms underlying the development of vascular injury in the diabetic patient is relevant to the understanding of the pathogenesis of cardiovascular disease in a significant proportion of hypertensive patients. Previous [2] and morc-recent [3] clinical trials have emphasized that hyperglycaemia is an independent risk factor for the development of cardiovascular disease. The fact that glucose uptake by vascular cells is largely insulin-independent renders vascular cells vulnerable to glucose-induced injury when the extracellular glucose concentration is elevated. The mechanism by which a high extracellular-intracellular flux of glucose contributes to the pathogenesis of vascular injury has not been confirmed, although numerous possibilities have been explored, including glucose-induced increases in intracellular sorbitol accumulation [4], the formation of advanced glycosylation end-products [5] and, more rcccntly, glucose-induced changes in cellular redox state [6].Attention has also been focused on a potcntial role for protein kinase C as a mediator of diabetes-induced vas–cular injury|| 7-14]. In this regard, protein kinase C is an attractive candidate, because it plays a pivotal role in the regulation of many biological functions within various cell types [15–17]. Moreover, vascular smooth