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Fig. 2 | Cell Communication and Signaling

Fig. 2

From: Common mechanisms underlying diabetic vascular complications: focus on the interaction of metabolic disorders, immuno-inflammation, and endothelial dysfunction

Fig. 2

The interaction mechanism of metabolic disorders, immuno-inflammation and endothelial dysfunction in DVCs. The metabolic disorder process, characterized by hyperglycemia and IR, involves glucose, lipid, and gut microbe metabolism. The immuno-inflammation process is activated by immunocytes, proinflammatory cytokines, and NETs. Then induced inflammation and redox injury cause damage to ECs and vessels. AGEs: advanced glycation end products; CXCL: chemokine (C-X-C motif) ligand; FFA: free fatty acid; IR: insulin resistance; LPS: lipopolysaccharide; Mφ: macrophages; MCP-1: monocyte chemoattractant protein 1; MDSCs: marrow-derived myeloid cells; NETs: neutrophil extracellular traps; NO: nitric oxide; NOX: NADPH oxidase; PGI-2: prostaglandin I-2; PKC: protein kinase C; RAGE: receptor of AGEs; SCFA: short-chain fatty acids; Th: T helper; TLR: Toll-like receptors; TMAO: trimethylamine-N-oxide; Treg: T regulatory cells; TxA2: thromboxane A2; VEGF: vascular endothelial growth factor

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Cell Communication and Signaling

ISSN: 1478-811X