Is it a high time to focus on iron-mediated pathology initiated by COVID-induced inflammation?

A comment to paper published in the current issue by Duca et al (Acta Biomed 2022; Vol. 93, N. 2: e2022057 - DOI 10.23750/abm.v93i2.12937 - https://mattioli1885journals.com/index.php/actabiomedica/article/view/12937). The paper demonstrated a link between deregulated iron homeostasis and hyperinflammation in nontreated COVID-19 patients. Iron homeostasis links two generally accepted COVID-initiated pathological events: hyperinflammation and abnormal fibrin clotting. Intensive research is needed to look for the ways how to support and recover FeH in COVID infected patients.

Hepcidin is a friend rather than a foe in COVID19-induced complications.

Clinical observations in concert with literary data demonstrate that detrimental complications of COVID19-induced pathology (acute respiratory distress syndrome, multi-organ failure, Kawasaki-like disease etc.), could result from a disturbance of local iron homeostasis (FeH) in damaged tissues followed by abnormal coagulation in small vessels. To resolve these complications the local FeH needs to be recovered. Hepcidin, as a master regulator of FeH is both a major player in the recovery and a marker of an efficacy of the restoration. Therefore, both local and systemic hepcidin levels could serve as a dynamic marker of disease progression (the more hepcidin the worse is disease) and treatment efficacy (after iron homeostasis is recovered hepcidin disappears). On the contrast, artificial attempts to suppress hepcidin expression directly or application of hepcidin antagonists could be detrimental. Overall, more comprehensive research of hepcidin role in COVID-19 pathology is needed.