Fig. 2

A potential biological function of the gut microbiota-microbial metabolites-mitochondria axis in the pathogenesis of DKD. In this hypothetical biological axis, with the deterioration of DM and digestion, degradation, and absorption of food by gut microbiota in the intestinal tract, the diversity and abundance of gut microbiota changed manifested by increased phylum Proteobacteria, Actinobacteria, Bacteroidetes and decreased phylum Firmicutes. Subsequently, various gut microbial metabolites are produced under the action of the gut microbiota and then released into the blood. These gut microbial metabolites, such as SCFAS, TMAO, PS and others, are transported to the kidney flowing the blood stream and interact with the mitochondria of kidney intrinsic cells. Metabolites of gut microbiota may lead to changes in mitochondrial function or disorder of mitochondrial quality control, thereby alleviating or accelerating the progression of DKD. SCFAs short-chain fatty acids, TMAO trimethylamine N-oxide, IS indoxyl sulfate, PS phenyl sulfate, Bas bile acids, K–W kimmelstiel–wilson, Scr serum creatinine, eGFR estimated glomerular filtration rate, ESRD end stage renal disease