Arterial calcification in diabetes.

Arterial calcification in diabetes.
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DOI:
10.1007/s11892-003-0049-2
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发表时间:
2003-02-01
影响因子:
4.2
通讯作者:
Moe, Sharon M
Moe, Sharon M
中科院分区:
医学2区
文献类型:
--
作者:
Chen, Neal X;Moe, Sharon M

文献摘要

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糖尿病与动脉粥样硬化性血管疾病和心血管死亡率增加有关。在糖尿病患者中,内侧钙化似乎是心血管死亡率的强有力的独立预测因素,尤其是在患有神经病变的患者中。最近的证据表明,糖尿病中的内侧钙化是一个活跃的、细胞介导的过程,类似于在终末期肾病 (ESRD) 患者中观察到的情况,其中血管平滑肌细胞 (VSMC) 表达许多骨基质蛋白,这些蛋白可促进或调节钙化过程。从糖尿病或 ESRD 患者获得的血管组织学切片中已证实存在几种骨相关蛋白(例如骨桥蛋白、骨唾液蛋白、碱性磷酸酶、1 型胶原、骨钙蛋白)。在体外实验中,高葡萄糖诱导培养的 VSMC 中的细胞增殖和骨桥蛋白的表达。缺氧与高血糖对 VSMC 具有累加效应。此外,尿毒症血清上调培养的 VSMC 中成骨细胞转录因子 Cbfa 1 和骨桥蛋白的表达。糖尿病血管钙化的发病机制尚不完全清楚,尽管高血糖和其他潜在因素可能通过将 VSMC 转化为成骨细胞样细胞而发挥重要作用。需要进一步了解糖尿病诱发这种并发症的机制,以设计有效的治疗策略来干预这一过程。
Diabetes is associated with an increased prevalence of atherosclerotic vascular disease and cardiovascular mortality. In diabetic patients, medial calcification appears to be a strong independent predictor of cardiovascular mortality, it occurs particularly in those with neuropathy. Recent evidence suggests that medial calcification in diabetes is an active, cell-mediated process, similar to that observed in patients with end-stage renal disease (ESRD), in which vascular smooth muscle cells (VSMCs) express a number of bone matrix proteins that act to either facilitate or regulate the calcification process. Several bone-associated proteins (e.g., osteopontin, bone sialoprotein, alkaline phosphatase, type 1 collagen, osteocalcin) have been demonstrated in histologic sections of vessels obtained from patients with diabetes or ESRD. In in vitro experiments, high glucose induced cell proliferation and expression of osteopontin in cultured VSMCs. Hypoxia had additive effects of hyperglycemia on VSMCs. In addition, uremic serum upregulates osteoblast transcription factor Cbfa 1 and osteopontin expression in cultured VSMCs. The pathogenesis of vascular calcification in diabetes is not completely understood, although high glucose and other potential factors may play an important role by transforming VSMCs into osteoblast-like cells. Further understanding of the mechanism by which diabetes induces this complication is needed to design effective therapeutic strategies to intervene with this process.