The role of short-chain fatty acids in kidney injury induced by gut-derived inflammatory response

被引:89
作者
Huang, Wei [1 ,2 ,3 ]
Zhou, Luping [3 ]
Guo, Hengli [1 ,2 ]
Xu, Youhua [1 ,2 ]
Xu, Yong [1 ,3 ]
机构
[1] Macau Univ Sci & Technol, Fac Chinese Med, Ave Wai Long, Taipa, Macao, Peoples R China
[2] Macau Univ Sci & Technol, State Key Lab Qual Res Chinese Med, Ave Wai Long, Taipa, Macao, Peoples R China
[3] Southwest Med Univ, Affiliated Hosp, Dept Endocrinol, Luzhou 646000, Sichuan, Peoples R China
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2017年 / 68卷
关键词
Gut-Kidney axis; Inflammation; Kidney injury; Short-chain fatty acids; NF-KAPPA-B; SODIUM-BUTYRATE; DIETARY FIBER; GASTROINTESTINAL-TRACT; HISTONE DEACETYLASES; EPITHELIAL-CELLS; GENE-EXPRESSION; NUCLEAR-FACTOR; T-CELLS; RECEPTOR;
D O I
10.1016/j.metabol.2016.11.006
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
It has been found that several circulating metabolites derived from gut microbiota fermentation associate with a systemic immuno-inflammatory response and kidney injury, which has been coined the gut-kidney axis. Recent evidence has suggested that short-chain fatty acids (SCFAs), which are primarily originated from fermentation of dietary fiber in the gut, play an important role in regulation of immunity, blood pressure, glucose and lipid metabolism, and seem to be the link between microbiota and host homeostasis. In addition to their important role as fuel for colonic epithelial cells, SCFAs also modulate different cell signal transduction processes via G-protein coupled receptors, and act as epigenetic regulators by the inhibition of histone deacetylase and as potential mediators involved in the autophagy pathway. Though controversial, an intimate connection between SCFAs and kidney injury has been revealed, suggesting that SCFAs may act as new therapeutic targets of kidney injury. This review is intended to provide an overview of the impact of SCFAs and the potential link to kidney injury induced by gut-derived inflammatory response. (C) 2016 Elsevier Inc. All rights reserved.
引用
收藏
页码:20 / 30
页数:11
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