No

Figure 1. Growth factors induce neovascularization but they also exert a number of other effects related to ischemic protection. The triggers and transduction mechanisms are equal to those secondary to pre- and postconditioning. Remarkably, this is true for a wide range of growth factors, cytokines and progenitor cells

Cytokines that have been studied for their capacity to recruit bone marrow derived progenitors, have pleiotropic effects as well. G-CSF [57, 58] as well as SCF [58] protect against ischemia reperfusion injury. Not only the cytokines that promote recruitment of progenitors exert this protection, but direct local administration of for instance EPCs at the time of reperfusion appear to offer protection against ischemia-reperfusion injury, presumably dependent on akt activation [59].

Both the functional consequences of pro-angiogenic growth factors, cytokines and cells, and the transduction pathways that serve as mediators, are exactly the same as those described for ischemic protection by pre- and postconditioning protocols (Figure 1). The parallels between the two may teach us more about the biology of ischemic protection but may also guide future therapy of ischemic cardiac disease.

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