Endothelial Progenitor Cells in Acute Ischemic Kidney Injury: Strategies for Increasing the Cells' Renoprotective Competence

Figure 1

Mechanisms that are potentially involved in the stimulation or inhibition of EPC-mediated renoprotection after acute renal ischemia. Agonistic effects on β1-integrins, as they are induced by the Epac-1 activator 8-O-cAMP, increase renoprotective effects of the cells by stimulating EPC homing to postischemic tissue sites. Another agonistic mechanism is increased production of vasostabilizing substances (e.g., VEGF) by the cells. Such increased production can be induced by cell pretreatment with the hormone melatonin. In contrast, inhibition of the VE- and N-cadherin system most likely results in decreased renoprotective competence of EPCs (for further explanation see text).