Figure 1.

Disrupted pathways in polycystic kidney disease (PKD) and potential therapeutic intervention with specific agents. Agents associated with potential therapeutic interventions are represented in red; ant = antagonist; inh = inhibitor. AC-VI = adenylate cyclase 6; Akt = protein kinase B; AMPK = AMP kinase; B-Raf = v-raf murine sarcoma viral oncogene homolog B1; CDK = cyclin-de-pendent kinase; CFTR = cystic fibrosis transmembrane conductance regulator; EGF = epidermal growth factor; EP 2 R = E-prostanoid receptor 2; ERK = extracellular signal-regulated protein kinase; GSK3 = glycogen synthase kinase 3; IGF1 = insulin-like growth factor 1; IP 3 R = inositol 1,4,5-trisphosphate receptor; MAPK = mitogen-activated protein kinase; mTOR = mammalian target for rapamycin; PC1 = polycystin-1; PC2 = polycystin-2; PDE = phosphodiesterase; PGE 2 = prostaglandin E2; PI3K = phosphatidylinositol 3-kinase; PKA = protein kinase A; PLA 2 = phospholipase A2; PLCγ = phospholipase C-γ2; R = somatostatin sst2 receptor; Rheb = ras homolog enriched in brain; RyR = ryanodine receptor; sFRP4 = secreted Frizzled-related protein 4; TK = tyrosine kinase; TNF-α = tumor necro-sis factor-α; TSC = tuberous sclerosis proteins tuberin (TSC2) and hamartin (TSC1); V2R = vasopressin V2 receptor; VEGF = vascular endothelial growth factor [9].