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. 2022 Jun 30;23(13):7261. doi: 10.3390/ijms23137261

Figure 1.

Figure 1

Pathophysiological mechanisms of hyperglycaemia-induced vascular damage. AGE, advanced glycation end products; PKC, protein kinase C; e-NOS, endothelial nitric oxide synthase; VEGF, vascular endothelial grow factor; ICAM-1, intercellular adhesion molecule-1; VCAM-1, vascular cell adhesion molecule-1; PUMA, p53 upregulated modulator of apoptosis; PTEN, phosphatase and TENsin homolog deleted on chromosome 10; TIGAR, TP53-Induced Glycolysis and Apoptosis Regulator; NO, nitric oxide; TxA2, Thromboxane A2; TF, tissue factor; GP, glycoprotein; MAPK, mitogen-activated protein kinase; BMK, big MAPK; PI3K, Phosphoinositide 3-kinases; NF-kB, nuclear factor kappa B; IRS-1, insulin receptor substrate 1; KLF-4, Kruppel Like Factor 4; ERK, extracellular signal-regulated kinase; BCL, B-cell lymphoma; Bft, Bacteroides fragilis toxin; MAC, membrane attack complex; LFA-1, lymphocyte function-associated antigen 1; MCP-1, monocyte chemoattractant protein-1; IL, interleukin; TNF, tumour necrosis factor.