Clustered view of pathways involved in AKI. A summarised overview of signalling cascades triggered by AKI leading ultimately to apoptosis and necrosis is shown. Based on the bioinformatics approach the Angiotensin-Aldosterone system, ROS, NFκB, glutamatergic signalling and cell death appear to be key targets for therapeutic intervention. Of these, ROS targeting approaches have failed to date and efforts should concentrate in selective ROS targeting. In this respect recent successful attempts have focused on mitochondrial ROS targeting. There is also evidence that targeting cell death and NFκB might be beneficial, although the complexity of the NFκB system requires exploration of more selective approaches. By contrast the role of glutamatergic signalling in AKI remains largely unexplored. The initial entry-point was selected by activating the RAAS axis, though it is known that different AKI-conditions can have other starting points within and outside the sequence of events depicted. Since pathway names can be ambiguous, the proteins involved and found in the most significant dataset of 1480 entries are listed as well. The protein coloration ranges from green (down-regulated) to red (up-regulated). Pathway names in green are evoked after transcriptional and translational events.