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10.3390/antiox9060540

http://scihub22266oqcxt.onion/10.3390/antiox9060540
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32575554!7346191!32575554
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suck abstract from ncbi


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pmid32575554      Antioxidants+(Basel) 2020 ; 9 (6): ä
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  • Targeting the Heme-Heme Oxygenase System to Prevent Severe Complications Following COVID-19 Infections #MMPMID32575554
  • Wagener FADTG; Pickkers P; Peterson SJ; Immenschuh S; Abraham NG
  • Antioxidants (Basel) 2020[Jun]; 9 (6): ä PMID32575554show ga
  • SARS-CoV-2 is causing a pandemic resulting in high morbidity and mortality. COVID-19 patients suffering from acute respiratory distress syndrome (ARDS) are often critically ill and show lung injury and hemolysis. Heme is a 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. Heme can be degraded by the anti-inflammatory enzyme heme oxygenase (HO) generating biliverdin/bilirubin, iron/ferritin, and carbon monoxide. We 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, we need to explore novel strategies to attenuate the pro-inflammatory, pro-thrombotic, and pro-fibrotic consequences of SARS-CoV-2 leading to morbidity and mortality. The heme-HO system represents an interesting target for novel "proof of concept" studies in the context of COVID-19.
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