A study on iron metabolism
Researchers have recently discovered a new mechanism of iron metabolism that will lead to an improvement in some pathological conditions which are associated with an erroneously regulation of the hormone that modulates the absorption and redistribution of iron within the entire body.
The study, published in Blood by the Italian researchers of the Vita San Raffaele University, stems from the analysis of two diseases, fibrodysplasia ossificans progressiva (FOP) and pulmonary arterial hypertension (PAH), which share some common aspects.
In particular, they share the alteration of the signaling of some molecules that regulate the expression of hepcidin, a hormone produced by the liver which modulates the absorption and redistribution of iron to the entire body.
The study analyzed the role of these molecules, and that of protein FKBP12, involved in the regulation of hepcidin levels, by using a number of drugs. By interacting with FKBP12, the latter alter their functioning against some receptors located on the cell membrane.
“With both approaches we have obtained an increase in the expression of hepcidin”, said Silvia Colucci, first author of the article, “as confirmed by the studies we have conducted on human hepatoma cell lines as well as mouse primary hepatocytes”.
There are several and important potential clinical implications, since “Low levels of hepcidin are responsible for diseases that result in an overload of iron and functional damage to many organs, including liver, heart, pancreas, which can be fatal if not adequately controlled”.