HMG-CoA reductase inhibitors (statins) increase endothelial progenitor cells via the PI 3-kinase/Akt pathway

Spectrum of Pleiotropic Effects of Statins in Heart Failure

“…[45,46] When inhibitors of PI-3 kinase were added the increase in EPCs was abolished. [44] In a murine infarct model, atorvastatin was found to augment the number of circulating EPCs after infarction. Interestingly, increased levels of circulating EPCs were not seen after treatment with atorvastatin in eNOS -/-mice, suggesting that eNOS has a role in mobilization of EPCs.…”

“…It is suggested that statins increase the levels of EPCs by acting through the PI3-kinase/AKT pathway. [44] Statins have been shown previously to activate PI-3 Kinase and AKT. [45,46] When inhibitors of PI-3 kinase were added the increase in EPCs was abolished.…”

Endothelial progenitor cells for cancer gene therapy

“…60 Statins can also mobilize a larger number of EPCs. 61 Of note, the vasculogenic rebound of tumors recovering from cytotoxic therapy involves the mobilization of EPCs. 62 This raises the possibility of harvesting EPCs after chemotherapy.…”

Neurorestorative treatment of stroke: Cell and pharmacological approaches

“…53 These proteins play an important role in regulating vascular and neurogenic, neuroprotective, and neurorestorative effects. 54,55 Specific cell populations and neurorestorative processes are targeted by statins. Statins increase brain endothelial cell expression of VEGF-VEGFR2 and eNOS and thereby activate the PI3K-AKT pathway, which regulates endothelial cell proliferation and migration and increases angiogenesis.…”