Published online Apr 15, 2022. doi: 10.4239/wjd.v13.i4.308
Peer-review started: May 9, 2021
First decision: July 3, 2021
Revised: August 9, 2021
Accepted: April 2, 2022
Article in press: April 2, 2022
Published online: April 15, 2022
Processing time: 339 Days and 19.5 Hours
Diabetic kidney disease (DKD) is one of the major chronic complications of diabetes mellitus (DM), as well as a main cause of end-stage renal disease. Over the last few years, substantial research studies have revealed a contributory role of gut microbiota in the process of DM and DKD. Metabolites of gut microbiota like lipopolysaccharide, short-chain fatty acids, and trimethylamine N-oxide are key mediators of microbial–host crosstalk. However, the underlying mechanisms of how gut microbiota influences the onset and progression of DKD are relatively unknown. Besides, strategies to remodel the composition of gut microbiota or to reduce the metabolites of microbiota have been found recently, representing a new potential remedial target for DKD. In this mini-review, we will address the possible contribution of the gut microbiota in the pathogenesis of DKD and its role as a therapeutic target.
Core Tip: This minireview consolidates the potential role of gut microbiota in the pathogenesis and as a therapeutic target of diabetic kidney disease. It is known that metabolites of gut microbiota such as trimethylamine N-oxide, short-chain fatty acids, and lipopolysaccharides are important mediators of microbial-host crosstalk. However, the main mechanism of how the gut microbiota specifically affects the occurrence and progress of diabetic kidney disease has not yet been fully explored.
