Cytokines, Atherogenesis, and Hypercatabolism in Chronic Kidney Disease: A Dreadful Triad
Cytokines, Atherogenesis, and Hypercatabolism in Chronic Kidney Disease: A Dreadful Triad
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DOI：
10.1111/j.1525-139x.2009.00585.x
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发表时间：
2009-07-01
影响因子：
1.6
通讯作者：
Stenvinkel, Peter
中科院分区：
文献类型：
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作者：
Carrero, Juan Jesus;Park, Sun-Hee;Stenvinkel, Peter
细胞因子簇一词表示涉及介导健康和疾病的众多过程的丰富的分子家族和相应的受体。在慢性肾脏病 (CKD) 的背景下，大多数细胞因子的生成和代谢受到干扰。现有证据表明，细胞因子失衡会导致常见 CKD 并发症的进展，例如动脉粥样硬化、矿物质骨疾病以及通过多效性作用导致的蛋白质能量浪费。肾病学家普遍存在误解，认为细胞因子 CKD 研究仅以白细胞介素 (IL) 和肿瘤坏死因子 (TNF)（主要是 IL-6 和 TNF-α）为代表。我们在此探讨有关各种细胞因子在尿毒症并发症中病理生理学作用的最新发现，并讨论如何将细胞因子用作 CKD 的新潜在治疗靶点。同时，我们对主要转化生长因子和趋化因子的最新发现进行了简要概述。
The term cytokine clusters denotes a copious family of molecules and correspondent receptors implicated in numerous processes mediating health and disease. In the context of chronic kidney disease (CKD), generation and metabolism of most of these cytokines are disturbed. Available evidence suggests that cytokine imbalances contribute to the progression of common CKD complications, such as atherosclerosis, mineral-bone disease, and protein-energy wasting via pleiotropic effects. The belief that cytokine CKD research is solely represented by interleukins (IL) and tumor-necrosis factors (TNF) (mainly IL-6 and TNF-alpha) is a common misconception among nephrologists. We here explore recent findings concerning the pathophysiological role of various cytokines in uremic complications, and discuss how cytokines could be used as novel potential therapeutic targets in CKD. At the same time, we provide a brief overview of current discoveries in the main transforming growth factors and chemokines.