9 December 2018
Global reach, higher impact
Int J Med Sci 2018; 15(8):816-822. doi:10.7150/ijms.25543
Intestinal dysbiosis activates renal renin-angiotensin system contributing to incipient diabetic nephropathy
1. Institute of Nephrology, Zhong Da Hospital, School of Medicine, Southeast University, Nanjing City, Jiangsu Province, China.
Considerable interest nowadays has focused on gut microbiota owing to their pleiotropic roles in human health and diseases. This intestinal community can arouse a variety of activities in the host and function as “a microbial organ” by generating bioactive metabolites and participating in a series of metabolism-dependent pathways. Alternations in the composition of gut microbiota, referred to as intestinal dysbiosis, are reportedly associated with several diseases, especially diabetes mellitus and its complications. Here we focus on the relationship between gut microbiota and diabetic nephropathy (DN), as the latter is one of the major causes of chronic kidney diseases. The activation of renin angiotensin system (RAS) is a critical factor to the onset of DN, and emerging data has demonstrated a provoking and mediating role of gut microbiota for this system in the context of metabolic diseases. The purpose of the current review is to highlight some research updates about the underlying interplay between gut microbiota, their metabolites, and the development and progression of DN, along with exploring innovative approaches to targeting this intestinal community as a therapeutic perspective in clinical management of DN patients.
Keywords: Gut microbiota, diabetic nephropathy, renin-angiotensin system
This is an open access article distributed under the terms of the Creative Commons Attribution (CC BY-NC) license (https://creativecommons.org/licenses/by-nc/4.0/). See http://ivyspring.com/terms for full terms and conditions.
How to cite this article:
Lu CC, Ma KL, Ruan XZ, Liu BC. Intestinal dysbiosis activates renal renin-angiotensin system contributing to incipient diabetic nephropathy. Int J Med Sci 2018; 15(8):816-822. doi:10.7150/ijms.25543. Available from http://www.medsci.org/v15p0816.htm