Table 2.
Origin | Types | Functions |
---|---|---|
Dietary tryptophan | Indoxyl sulfate | a. Inhibiting endothelial cell proliferation and damaging endothelial progenitor cells by inducing oxidative stress and inflammation41 b. Increasing TF/FVII levels by upregulating the AhR-STUB1-TF axis40,42 c. Activating platelets by inducing oxidative stress-mediated p38 MAPK activation43 |
Indole-3-acetic acid | a. Inducing COX-2 expression by activating AhR/p38 MAPK/NF-κB signaling pathways, which led to inflammation and endothelial injury44 b. Increasing TF/FVII levels by upregulating the AhR-STUB1-TF axis40,42 c. Activating platelets by inducing oxidative stress-mediated p38 MAPK activation43 |
|
Kynurenine pathway–derived uremic toxins | a. Inducing inflammation and oxidative stress by activating AhR, which caused endothelial dysfunction and TF overexpression45 b. Causing coagulation factors disorder40,a |
|
Phenylalanine/tyrosine | Phenylacetylglutamine | Inducing platelet hyperreactivity by activating α2A-, α2B-, β2-adrenergic receptors46 |
P-cresol sulfate | Promoting MP release from endothelial cells47,a | |
P-cresol glucuronide | Promoting MP release from endothelial cells47,a | |
Choline/phosphatidylcholine | Trimethylamine N-oxide | Promoting IP3-mediated Ca2+ release, leading to platelet hyperreactivity48 |
TF, tissue factor; FVII, coagulation factor VII; AhR, aryl hydrocarbon receptor; STUB1, stress-induced phosphoprotein 1 homologous and U-box containing protein 1; p38 MAPK, p38 mitogen-activated protein kinase; NF-κB, nuclear factor-kappaB; MPs, microparticles; IP3, 1,4,5-trisphosphate.
Indicates that the underlying mechanism has not been elucidated.