Publications by authors named "Alcira Beatriz Nesse"
Article Synopsis
- Regulation of iron (Fe) levels is crucial for processes like red blood cell production (erythropoiesis) and to prevent toxicity, with hepcidin being the key regulatory peptide produced by the liver that controls Fe absorption and release.
- Erythropoietin (Epo), a glycoprotein that supports red blood cell development, directly inhibits hepcidin expression in liver cells (HepG2), resulting in lowered intracellular Fe levels through the activation of specific signaling pathways, particularly JAK2 and PI3K/AKT/mTOR.
- Epo's effects on hepcidin also involve modulation of transcription factors, decreasing the activity of C/EBP-α while enhancing the inhibitory
Many patients under therapy with recombinant human erythropoietin (rhuEPO) show resistance to the treatment, an effect likely associated with the accumulation of tissue factors, especially in renal and cardiovascular diseases. Hyperhomocysteinemia due to high serum levels of homocysteine has been suggested among the risk factors in those pathologies. Its main effect is the N-homocysteinylation of proteins due to the interaction between the highly reactive homocysteine thiolactone (HTL) and lysine residues.
View Article and Find Full Text PDFIt is now recognized that in addition to its activity upon erythroid progenitor cells, erythropoietin (Epo) is capable of stimulating survival of different non-erythroid cells. Since stimulation of erythropoiesis is unwanted for neuroprotection, Epo-like compounds with a more selective action are under investigation. Although the carbamylated derivative of erythropoietin (cEpo) has demonstrated non-hematopoietic tissue protection without erythropoietic effect, little is known about differential mechanisms between Epo and cEpo.
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