Figure 1.

Schematic representation of some of the signaling intermediates potentially involved in regulation of inflammatory response after UUO. UUO induces IL-1β and TNF-α expression, leading to NF-κB activation. UUO also induces both oxidative stress and increased Angiotensin II (Ang II) levels. Ang II also activate the transcription factor NF-κB, both directly and indirectly, by promoting oxidative stress, which in turns activate Ang II by regulating angiotensinogen expression. TGF-β activates NF-κB through I-κB inhibition, a mechanism shared by TNF-α. NF-κB activation concludes in IL-1β and TNF-α expression enhancing NF-κB activation. Also NF-κB controls the expression of genes encoding pro-inflammatory cytokines, adhesion molecules and iNOS.