Chao Chia-Ter, Chiang Chih-Kang
Renal Division, Department of Internal Medicine, National Taiwan University Hospital Jin-Shan Branch, New Taipei City, Taiwan; Department of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan; Graduate Institute of Toxicology, National Taiwan University College of Medicine, Taipei, Taiwan.
Department of Internal Medicine, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan; Graduate Institute of Toxicology, National Taiwan University College of Medicine, Taipei, Taiwan; Department of Integrative Diagnostics and Therapeutics, National Taiwan University Hospital, National Taiwan University College of Medicine, Taipei, Taiwan.
J Ren Nutr. 2015 Mar;25(2):155-9. doi: 10.1053/j.jrn.2014.10.010. Epub 2014 Dec 12.
The prevalence of end-stage renal diseases is currently on the rise globally, and finding the way to curb this tide is urgently needed. Tubulointerstitial fibrosis is a common pathway for essentially all the nephropathy categories known to date, and the manifestations of renal fibrosis include excessive deposition of extracellular matrix with distortion of renal microstructures and functional deterioration. Uremic toxins have been gradually found to play an important role in the development of progressive renal fibrosis, with protein-bound indoxyl sulfate, p-cresol, and p-cresyl sulfate receiving the most attention. However, the contribution of oxidative stress among the pathogenesis of uremic toxins and renal fibrosis has not been evaluated much until recently. In this review, we will discuss about the nature and sources of oxidative stress in the kidney and how uremic toxins use oxidative stress to orchestrate the processes of renal fibrosis.
目前,终末期肾病在全球的患病率呈上升趋势,因此迫切需要找到遏制这一趋势的方法。肾小管间质纤维化是迄今已知的所有肾病类型的共同途径,肾纤维化的表现包括细胞外基质过度沉积、肾微结构扭曲和功能恶化。人们逐渐发现尿毒症毒素在进行性肾纤维化的发展中起重要作用,其中与蛋白结合的硫酸吲哚酚、对甲酚和硫酸对甲酚受到的关注最多。然而,直到最近,氧化应激在尿毒症毒素和肾纤维化发病机制中的作用才得到较多评估。在这篇综述中,我们将讨论肾脏中氧化应激的性质和来源,以及尿毒症毒素如何利用氧化应激来调控肾纤维化过程。