Erythroferrone (ERFE) is a hormone released in the bone marrow by erythroblasts in response to erythropoietin, which regulates the release of iron accumulation by its action on hepcidin, acting on hepatocytes to suppress hepcidin hormone expression. Erythroferrone is one of the possible therapeutic biomarkers for determining the activity of erythropoiesis in patients with blood disorders with respect to iron imbalance. Since Dr. Leon Kautz and colleagues were discovered in 2014 and until now there have been inadequate studies of Erythroferrone among humans, most studies are performed in animals. The role of Erythroferrone hormone as the erythroid hepcidin and iron metabolism regulator during thalassemia, inflammatory anaemia, and iron deficiency anaemia is briefly discussed in this chapter. Through a search using the following electronic databases, studies were found in this review: PubMed, Academia, Scopus, Google Scholar, and another open source database. Conclusion: Several studies have concluded that erythroferrone levels in the blood are higher in people with inflammatory thalassemia and iron deficiency anaemia than in people without thalassemia and iron deficiency anaemia. Awareness of the mechanisms of erythroferrone as an erythroid hepcidin and iron metabolism regulator during thalassemia and in iron deficiency anaemia is essential for both conditions in diagnosis and treatment. In cases of iron deficiency anaemia and thalassemia disease, erythroferrone hormone can act as a potential factor in the physiological suppression of hepcidin and play a key role in the treatment process among those patients with iron deficiency or iron overload status. However, there are few studies on the role of ERFE in humans so far since it has recently been discovered and continues to be studied, and most animal studies are carried out.
Author (s) DetailsAsaad Ma. Babker
Department of Medical Laboratory Sciences, College of Health Sciences, Gulf Medical University, Ajman, United Arab Emirates.
View Book :- https://stm.bookpi.org/HMMR-V3/issue/view/32
No comments:
Post a Comment