Published online Aug 26, 2015. doi: 10.4331/wjbc.v6.i3.78
Peer-review started: January 28, 2015
First decision: March 6, 2015
Revised: April 20, 2015
Accepted: May 16, 2015
Article in press: May 18, 2015
Published online: August 26, 2015
Processing time: 211 Days and 3 Hours
Iron metabolism is regulated on the cellular and the systemic level. Over the last decade, the liver peptide “hepcidin” has emerged as the body’s key irons store regulator. The long postulated “erythroid regulator of iron”, however, remained elusive. Last year, evidence was provided, that a previously described myokine “myonectin” may also function as the long sought erythroid regulator of iron. Myonectin was therefore re-named “erythroferrone”. This editorial provides a brief discussion on the two functions of erythroferrone and also briefly considers the emerging potential role of transferrin receptor 2 in erythropoiesis.
Core tip: Iron metabolism is regulated on the cellular and the systemic level. Over the last decade, the small, 25-amino-acid liver peptide “hepcidin” has emerged as the body’s key irons store regulator. The long postulated “erythroid regulator of iron”, however, remained elusive. Several candidates have been suggested in the literature, however all had to be dismissed. Last year, evidence was provided, that erythroferrone, a previously described myokine, may also function as the long sought erythroid regulator of iron. While erythroferrone appears to be an important iron regulator for erythropoiesis, transferrin receptor 2 also emerges as a player in this regulation.