Endogenous Inhibitors of Kidney Inflammation.

Endogenous Inhibitors of Kidney Inflammation.
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DOI:
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发表时间:
2015-10
期刊:
Journal of nephrology research
影响因子:
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通讯作者:
Jessica Trostel;G. Garcia
Jessica Trostel;G. Garcia
中科院分区:
其他
文献类型:
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作者:
Jessica Trostel;G. Garcia

文献摘要

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虽然炎症是对病原体入侵和组织损伤的生理反应,但它也可能导致显著的组织损伤。因此,必须仔细调节炎症反应,以防止对重要器官的严重炎症损伤。通常,局部内源性调节机制调节反应的大小,使得损伤性病症得到解决并保持体内平衡。抑制炎症的体液机制包括糖皮质激素、抗炎细胞因子(如IL-10和转化生长因子-β(TGF-β))和可溶性细胞因子受体;其他介质促进组织愈合,如脂氧素和消退素。越来越多的证据表明,炎症在心脏病、癌症、中风、糖尿病、肾脏疾病、败血症和几种纤维增生性疾病的发展和进展中起关键作用。因此,了解调节炎症的机制可能为抑制几种疾病的进展提供治疗靶点。本文综述了几种新的内源性抗炎介质在肾脏损伤保护中的意义以及这些调节分子作为肾脏炎症性疾病治疗靶点的潜力。
Although inflammation is the physiological response to pathogen invasion and tissue damage, it can also be responsible for significant tissue damage. Therefore, the inflammatory response must be carefully regulated to prevent critical inflammatory damage to vital organs. Typically, local endogenous regulatory mechanisms adjust the magnitude of the response such that the injurious condition is resolved and homeostasis is mantained. Humoral mechanisms that restrain or inhibit inflammation include glucocorticoid hormones, anti-inflammatory cytokines such as IL-10 and transforming growth factor-β (TGF-β), and soluble cytokine receptors; other mediators facilitate tissue healing, like lipoxins and resolvins. There is growing evidence that inflammation plays a critical role in the development and progression of heart disease, cancer, stroke, diabetes, kidney diseases, sepsis, and several fibroproliferative disorders. Consequently, understanding the mechanisms that regulate inflammation may offer therapeutic targets for inhibiting the progression of several diseases. In this article, we review the significance of several novel endogenous anti-inflammatory mediators in the protection from kidney injury and the potential of these regulatory molecules as therapeutic targets for treatment of kidney inflammatory diseases.