Targeting gut microbiota and its associated metabolites as a potential strategy for promoting would healing in diabetes

Figure 1 Gut microbiota and its associated metabolites like short chain fatty acids, hydrogen sulfide, tryptophan, and bile acids. SCFA: Short chain fatty acids; BA: Bile acids; TRP: Tryptophan; H₂S: Hydrogen sulfide. This figure was created using BioRender.com.

Figure 2 Metabolites regulate the healing of diabetic wounds through various pathways. The metabolites such as chain fatty acids, hydrogen sulfide, tryptophan, and bile acids mediated by gut microbiota (GM) have a positive regulatory ability on the inhibiting inflammation and apoptosis, reducing oxidative stress, regulating blood glucose levels and promoting reepithelialization and angiogenesis. While the type 2 diabetes mellitus patients are accompanied by intestinal microbiota disorders and an increased intestinal permeability, which will cause the down-regulation of GM metabolites entering the circulatory system, and may eventually further aggravate diabetes wounds. SCFA: Short chain fatty acids; BA: Bile acids; TRP: Tryptophan; ZO-1: Zonula Occludens-1; HDACs: Histone deacetylases; MDA: Malondialdehyde; GSH: Glutathione; GM: Gut microbiota; 5-HT: 5-hydroxytryptamine; M1: M1 macrophages; M2: M2 macrophages; IDO: Indoleamine 2:3-dioxygenase; PYY: Peptide YY; GLP-1: Glucagon-like peptide-1; SOD: Superoxide dismutase; ROS: Reactive oxygen species; Ang-1: Angiopoietin-1; VEGF: Vascular endothelial growth factor; eNOS: Endothelial nitric oxide synthase; AKT: Protein Kinase B; DNMT1: DNA methyltransferase 1; NETs: Neutrophil extracellular traps; H₂S: Hydrogen sulfide. This figure was created using BioRender.com.