COVID-19 patients suffering from Acute Respiratory Distress Syndrome (ARDS) are often critically ill and show lung injury and hemolysis. Heme is as prosthetic moiety crucial for the function of a wide variety of heme-proteins, including hemoglobin and cytochromes. However, injury-derived free heme promotes adhesion molecule expression, leukocyte recruitment, vascular permeabilization, platelet activation, complement activation, thrombosis, and fibrosis.
In a publication in Antioxidants, Frank Wagener, Peter Pickkers and internationals collaborators postulate that the heme-HO system represents an interesting target for novel “proof of concept” studies in the context of COVID-19. In particular, heme can be degraded by the anti-inflammatory enzyme heme oxygenase (HO) generating biliverdin/bilirubin, iron/ferritin and carbon monoxide. The RIMLS researchers therefore postulate that free heme contributes to many of the inflammatory phenomena witnessed in critically ill COVID-19 patients, whilst induction of HO-1 or harnessing heme may provide protection. HO-activity not only degrades injurious heme, but its effector molecules possess also potent salutary anti-oxidative and anti-inflammatory properties. Until a vaccine against SARS-CoV-2 becomes available, novel strategies need to be explored to attenuate the pro-inflammatory, pro-thrombotic and pro-fibrotic consequences of SARS-CoV-2 leading to morbidity and mortality.
Publication in Antioxidants, by Frank Wagener, theme Reconstructive and regenerative medicine, and colleagues.
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