ERK- and Akt-Dependent Neuroprotection by Erythropoietin (EPO) against Glyoxal-AGEs via Modulation of Bcl-xL, Bax, and BAD

Abstract

These data demonstrate that exogenous EPO significantly attenuates the retinal neuronal cell death induced by glyoxal-AGEs by promoting antiapoptotic and suppressing apoptotic proteins. EPO/EPO receptor signaling through ERK and Akt pathways is pivotal in EPO neuroprotective mechanisms.