Figure 1: Apoptotic stimuli activate caspases, triggering the proteolysis of a large number of intracellular substrates. The cleavage of many of these, including iCAD and lamins, is necessary for the morphological and biochemical changes of apoptosis. Other substrates have as yet undefined roles, while the cleavage of iPLA2 is critical for the paracrine signalling that induces compensatory proliferation. Cleavage of iPLA2 increases its activity, so raising the levels of PGE2 and LPC. PGE2 in turn activates EP2 G protein-coupled receptors on stem or progenitor cells. Intracellular signalling downstream of EP2 activates β-catenin and leads to cell proliferation. LPC and ATP may indirectly induce compensatory proliferation through the recruitment of macrophages.