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. 2022 Jun 17;13:908219. doi: 10.3389/fimmu.2022.908219

Figure 4.

Figure 4

The potential mechanism between gut dysbiosis and DKD. The decreased glomerular filtration rate of DKD patients leads to the accumulation of metabolic waste, which enters the intestinal lumen through the intestinal wall and results in gut dysbiosis. The composition and function of gut microbiota in patients with DKD significantly varied, resulting in the destruction of intestinal epithelial barrier function. Gut microbiota metabolites enter the blood and further aggravate the progression of DKD through a variety of pathways. TMAO, trimethylamine-N-oxide; PS, phenyl sulfate; SCFAs, short-chain fatty acids; BAs, bile acids; LPS, lipopolysaccharide; NF- κB, nuclear factor kappa-B; MAPK, mitogen-activated protein kinases; G-protein-coupled receptors (GPRs), such as GPR41 and GPR43; GLP-1, glucagon-like peptide-1; PYY, peptide YY; HADC, histone deacetylases; TGR5, Takeda G-protein receptor 5; FXR, farnesoid X receptor; TLR, toll-like receptors; JNK, c-Jun N-terminal kinase; IKK, IkappaB kinase; IR, insulin resistance; GBM, glomerular basement membrane; DKD, diabetic kidney diseases.