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首页> 外文期刊>Journal of pharmacology & toxicology. >Mechanisms of Endothelial Dysfunction: Clues from Cyclosporine*
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Mechanisms of Endothelial Dysfunction: Clues from Cyclosporine*

机译：内皮功能障碍的机制：来自环孢菌素的线索*

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There has been recent interest in the role of the kidney in the regulation of metabolic byproducts thought to be involved in the induction of endothelial dysfunction. The symptoms include increased blood pressure, decreased kidney function, increase in serum markers such as transforming growth factor beta, reactive oxygen species, asymmetric dimethylated arginine and an increase in the prothrombic and inflammatory state of the vasculature. Pathologies that exhibit this unique set of physiological findings include such diseases as diabetes, hypertension and other types of cardiovascular disease. Interestingly, the side effects of cyclosporine (CsA) treatment or more specifically, CsA induced nephropathy, exhibit many of the same type of symptoms. CsA was introduced as a way to inhibit the immune system for the purposes of increasing the long-term success of organ transplantations. However, as the CsA doses were increased to gain a higher level of immime system suppression, the greater the incidence of CsA induced side effects. When these are examined, there is a strong resemblance to the group of physiological findings in endothelial dysfunction. In what was supposed to be an immune system suppressant, CsA appears to have the ability, in high doses, to initiate an inflammatory response. This response seems to implicate a mechanism with its roots in the calcineurinuclear factor of activated T-cells (NFAT) pathway. Kidney dysfunction and hypertension are precursors to endothelial dysfunction and the calcineurin/NFAT pathway, which is disrupted by CsA, is strongly implicated in the process and may be a key to tmderstanding the pathophysiology.
机译：最近，人们对肾脏在调节代谢副产物中的作用感兴趣，这些副产物被认为与诱导内皮功能障碍有关。症状包括血压升高，肾功能下降，血清标志物（例如转化生长因子β），活性氧，不对称的二甲基化精氨酸增加以及脉管系统的血栓形成和炎症状态增加。表现出这种独特的生理发现的病理包括诸如糖尿病，高血压和其他类型的心血管疾病的疾病。有趣的是，环孢素（CsA）治疗或更确切地说是CsA诱导的肾病的副作用表现出许多相同类型的症状。引入CsA作为抑制免疫系统的一种方法，目的是增加器官移植的长期成功率。但是，随着CsA剂量的增加，以获得更高的免疫系统抑制水平，CsA引起的副作用发生率也更高。当检查这些时，与内皮功能障碍的一组生理学发现非常相似。在被认为是一种免疫系统抑制剂的情况下，CsA似乎具有大剂量引发炎症反应的能力。这种反应似乎暗示其根源于活化T细胞（NFAT）途径的钙调神经磷酸酶/核因子的机制。肾脏功能障碍和高血压是内皮功能障碍的前兆，而钙调神经磷酸酶/ NFAT途径（被CsA破坏）与该过程密切相关，并且可能是理解病理生理的关键。

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