Table 4.

Most important affected pathophysiologic mechanisms

Affected MediatorsEffectToxinConfirmed in Two or More StudiesRelated to InflammationRelated to Fibrosis
α-Smooth muscle actin36,38,40,49IS, PCSXX
Cytokine generation34,35IS, PCSXX
E-cadherin36,38IS, PCSXX
Nuclear Factor (erythroid-derived 2) -like 249,50ISXX
Extracellular-regulated kinase 1/244PCSX
Fibronectin36IS, PCSX
Heme oxygenase-149,50ISXX
Intercellular Adhesion Molecule-147ISX
Inflammatory genes34IS, PCSX
Insulin receptor substrate-144PCSX
Klotho39IS, PCSX
Mitogen-activated protein kinase: MEK 1/2; p3835ISX
Multidrug resistance-associated protein-248IS
NADPH oxidase27,30,45IS, PCSXX
Nuclear Factor-κB35ISX
Organic Anion Transporters40,48ISX
Osteoblast-specific proteins40ISX
Phosphoinositide 3-kinase44PCSX
Protein kinase B/Akt44PCSX
Renin-angiotensin-aldosterone system36IS, PCSXX
E-selectin30ISX
Senescence proteins41aIS
Smad2/3 and Smad436,43IS, PCSXX
Snail36IS, PCSX
Tissue factor46IS
Transforming Growth Factor-β36,40,43,49IS, PCSXX
Zonula occludens-138ISX
  • IS, indoxyl sulfate; PCS, p-cresyl sulfate.

  • a Senescence proteins: senescence-associated β-galactosidase, 16INK4a, p21WAF1/CIP1, p53, and retinoblastoma protein.