The term translational research is used to describe the application of discoveries made in the research laboratory to medical diagnosis and treatment. The ongoing story of the understanding of hepcidin is a good example of this process.
A couple of decades ago no one knew of the existence of the small peptide hepcidin, but in 2001 US scientists reported its discovery in the urine of healthy humans. After its discovery, international research interest in hepcidin grew year on year as its pivotal role in body iron regulation became clear.
Confirmation that hepcidin was involved in one way or another in the pathogenesis of iron-related disease (eg iron deficiency anaemia, anaemia of inflammation, thalassaemia, haemochromatosis) soon suggested that measurement of hepcidin could have clinical value. Development of the first enzyme-linked immunosorbent assay (ELISA) for hepcidin facilitated measurement of serum hepcidin in the routine clinical laboratory, enabling translational hepcidin research. One early example describes a translational hepcidin study designed to assess the ability of a hepcidin ELISA to identify the cause of anaemia among the critically ill.1
Hepcidin, a 25 amino acid (cysteine-rich) peptide, is the principal iron regulatory hormone. It is derived from a much larger (84 amino acid) peptide, called preprohepcidin, synthesised in hepatocytes. By two-stage enzymatic cleavage in the cytosol of hepatocytes, preprohepcidin is converted first to the prohormone prohepcidin and then to the biologically active hormone hepcidin, which is exported from hepatocytes to circulate in blood plasma. It is readily filtered at the glomerulus and excreted in urine.
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