Erythropoietin (EPO) promotes cell growth, differentiation, migration, and survival. Among the acute effects of EPO, antiapoptosis is predominant. Apoptosis is one of the major forms of cell death. EPO prevents apoptosis following injury in various organs including heart, brain, kidney, and liver. The late-phase effects of EPO include anti-inflammation, recruitment of endothelial-progenitor cells (EPC), and neovascularization. Plasma EPO is increased in response to hypoxia. The increased EPO is mainly produced by the kidney, although many tissues synthesize EPO that acts locally. EPOR (EPO receptor) is extensively expressed in various tissues, including endothelial cells, cardiomyocytes, and neuronal cells. Recombinant human EPO has been shown to protect the heart and the brain against ischemia or ischemia-reperfusion injury through antiapoptosis, anti-inflammation, EPC recruitment, and neovascularization. Moreover, recent studies, by using transgenic EPOR-rescued mice, indicate that endogenous EPO plays a role in preventing tissue injury from hypoxia or ischemia-reperfusion. The protective effect of EPO is likely mediated by survival signaling pathways including phosphatidylinositol 3-kinases and extracellular-signal-regulated kinases.
|Original language||English (US)|
|Title of host publication||Textbook of Nephro-Endocrinology|
|Number of pages||7|
|State||Published - Jan 1 2009|
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