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* Correspondence: a.koch@iem.unikiel.de Joint Section of Maritime Medicine, Naval Institute of Maritime Medicine and Christian-Albrechts-University Kiel, Kiel, Germany Full list of author information is available at the end of the article Introduction In the current pandemic of severe acute respiratory syndrome corona virus 2 (SARSCoV-2), the therapeutic administration of oxygen is a common procedure in order to mitigate patient’s hypoxia in the course of severe corona virus disease 2019 (COVID-19) pneumonia. However, additional oxygen causes a variety of well-known side-effects, impacting a number of systems regulating cardiovascular and respiratory homeostasis as well as reactive oxygen species (ROS)-production via oxidative stress. In this article, we want to focus on intermittent changes in lung and tissue oxygenation, as changes in local pO2 may be able to trigger one of the key effectors of cellular oxygen-sensing, hypoxia-inducible factor-1α (HIF-1α) and, in downstream, the expression of angiotensin-converting enzyme-2 (ACE2) and Furin. Recently, evidence has been found that the ACE2-receptor in lung tissue, in combination with Furin, is essential for the development of COVID-19 [1–3]. Besides, there is also new information, that in contrast a severe course of lung complication of COVID-19 is correlated with reduced ACE2 on the cell surface due to shedding of the ACE2-receptor from the cell surface [4] and thus, with an insufficient angiotensin-(2) (AT2)-conversion to angiotensin-(1-7) (AT1-7). This finding, that reduced ACE2 on lung cell surfaces is correlated with lung damage due to an uncontrolled renin-angiotensin system (RAS) cascade, is supported by recent data about effects of long-lasting hyperoxia on pulmonary tissue [5–10]. Thus, in the course of COVID-19, ACE2 plays a complex role: high levels of ACE2receptors on the cell surface in combination with Furin may facilitate SARS-Cov2-

intensive care medicine experimental

The conundrum of using hyperoxia in COVID-19 treatment strategies: may intermittent therapeutic hyperoxia play a helpful role in the expression of the surface receptors ACE2 and Furin in lung tissue via triggering of HIF-1α?