Fig. 1

Possible mechanisms mediating PTX’s renal effects. AC, adenylate cyclase; aPKA, active protein kinase A; α-SMA, α-smooth muscle actin; ATP, adenosine triphosphate; cAMP, cyclic adenosine-3,5-monophosphate; CRE, cAMP response element; CREB, cAMP-response element binding protein; CTGF, connective tissue growth factor; CX3CL1, fractalkine; FN, fibronectin; GPCP, G-protein-coupled receptor; Grb2, growth factor receptor-bound protein 2; ICAM-1, intercellular adhesion molecule-1; IκB, inhibitory protein of NF-κB (p65/p50 heterodimer); IKK, IκB kinase; iPKA, inactive protein kinase A; MAPK, mitogen activated protein kinase; MCP-1, monocyte chemoattractant protein-1; P, phosphorylation; PDE, phosphodiesterase; PDGF, platelet-derived growth factor; PI3K, phosphatidylinositol 3-kinase; Sos, son of sevenless; TGF-β1, transforming growth factor-β1; TNF-α, tumor necrosis factor-α; PTX, pentoxifylline; TRADD, TNFR1-associated death domain protein; TRAF2, TNF receptor-associated factor 2; U, ubiquitination. Dash lines denote inhibitory pathways initiated by PTX from the leftmost side