PubMed · 3101432
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A Kurtz. 1987. Erythropoietin: structure, function, origin.. https://pubmed.ncbi.nlm.nih.gov/3101432/
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INTRODUCTION: The pathogenesis of anemia and other erythroid dysphasia are mains poorly understood, primarily due to limited knowledge about the differentiation processes and regulatory mechanisms governing erythropoiesis. Erythropoiesis is a highly complex and precise biological process, that can be categorized into three distinct stages: early erythropoiesis, terminal erythroid differentiation, and reticulocyte maturation, and this complex process is tightly controlled by multiple regulatory factors. Emerging evidence highlights the crucial role of epigenetic modifications, particularly histone modifications, in regulating erythropoiesis. Methylation and acetylation are two common modification forms that affect genome accessibility by altering the state of chromatin, thereby regulating gene expression during erythropoiesis. DISCUSSION: This review systematically examines the roles of histone methylation and acetylation, along with their respective regulatory enzymes, in regulating the development and differentiation of hematopoietic stem/progenitor cells (HSPCs) and erythroid progenitors. Furthermore, we discuss the involvement of these histone modifications in erythroid-specific developmental processes, including hemoglobin switching, chromatin condensation, and enucleation.Conclusions This review summarizes the current understanding of the role of histone modifications in erythropoiesis based on existing research, as a foundation for further research the mechanisms of epigenetic regulatory in erythropoiesis.
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In has been long recognized that erythropoiesis in adults is under control of erythropoietin, a glycoprotein produced mainly by adult kidneys in inverse relation to oxygen availability. Increasing evidence indicates nowadays that EPO is also an essential growth factor for red cell precursors at different sites of fetal erythropoiesis. The primary site of EPO production during fetal and neonatal life is the liver, and the fetus has been shown to be able to increase EPO production in response to hypoxia through intrinsic oxygen sensing mechanisms of hepatocytes. Thus despite different sites of both erythropoiesis and EPO production a similar oxygen dependent feedback control of red cell formation appears to operate during all stages of development. EPO levels in fetal blood are potentially useful parameters of fetal stress, and, as in adults, the availability of recombinant EPO raises the possibility to modulate erythropoiesis in the perinatal period.