Ferroptosis - a link between iron biology, aging and COVID-19?

Severe form of COVID-19 is more common in the elderly and although it may include a variety of extrapulmonary manifestations, respiratory dysfunction is primarily present, which includes iron dy- shomeostasis. The aging process is characterized by a chronic pro-inflammatory condition of a milder type, and COVID-19 by strong acute inflammation, both resulting in changes in iron metabolism. A new, iron-dependent form of programmed cell death, ferroptosis, is associated with iron dyshomeosta- sis. The main features of ferroptosis include intracellular iron overload, inhibition of the cellular GSH / GPX4 system, and accumulation of lipid reactive compounds. Clinical manifestations of COVID-19 and changes during aging include GSH depletion, GPX4 inactivation, changes in iron metabolism markers as well as markers of enhanced lipid peroxidation. There is therefore a possibility that SARS- CoV-2 may cause feroptotic death of lung cells but also cells of other organs. This review considers the molecular mechanisms of ferroptosis, their relationship to the aging process and the pathogenesis of COVID-19, and the consideration of ferroptosis as a factor linking aging and the pathogenesis of COVID-19