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. 2014 May 8;25(9):1897–1907. doi: 10.1681/ASN.2013101062

Table 4.

Most important affected pathophysiologic mechanisms

Affected Mediators Effect Toxin Confirmed in Two or More Studies Related to Inflammation Related to Fibrosis
α-Smooth muscle actin36,38,40,49 IS, PCS X X
Cytokine generation34,35 IS, PCS X X
E-cadherin36,38 IS, PCS X X
Nuclear Factor (erythroid-derived 2) -like 249,50 IS X X
Extracellular-regulated kinase 1/244 PCS X
Fibronectin36 IS, PCS X
Heme oxygenase-149,50 IS X X
Intercellular Adhesion Molecule-147 IS X
Inflammatory genes34 IS, PCS X
Insulin receptor substrate-144 PCS X
Klotho39 IS, PCS X
Mitogen-activated protein kinase: MEK 1/2; p3835 IS X
Multidrug resistance-associated protein-248 IS
NADPH oxidase27,30,45 IS, PCS X X
Nuclear Factor-κB35 IS X
Organic Anion Transporters40,48 IS X
Osteoblast-specific proteins40 IS X
Phosphoinositide 3-kinase44 PCS X
Protein kinase B/Akt44 PCS X
Renin-angiotensin-aldosterone system36 IS, PCS X X
E-selectin30 IS X
Senescence proteins41a IS
Smad2/3 and Smad436,43 IS, PCS X X
Snail36 IS, PCS X
Tissue factor46 IS
Transforming Growth Factor-β36,40,43,49 IS, PCS X X
Zonula occludens-138 IS X

IS, indoxyl sulfate; PCS, p-cresyl sulfate.

a

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

HHS Vulnerability Disclosure