Heme oxygenase-1 modulation: A potential therapeutic target for COVID-19 and associated complications

被引:41
作者
Singh, Devendra [1 ]
Wasan, Himika [1 ]
Reeta, K. H. [1 ]
机构
[1] All India Inst Med Sci, Dept Pharmacol, New Delhi, India
关键词
SARS-CoV-2; COVID-19; Heme Oxygenase-1; Antiviral activity; Type-1; IFNs; Inflammation; HO-1 promoter polymorphism; Coagulopathy; HEPATITIS-C VIRUS; PROMOTER MICROSATELLITE POLYMORPHISM; CORONARY-ARTERY-DISEASE; CARBON-MONOXIDE; GENE PROMOTER; ANTIVIRAL ACTIVITY; MAPK/NRF2; PATHWAY; HCV REPLICATION; RAT-BRAIN; IN-VITRO;
D O I
10.1016/j.freeradbiomed.2020.10.016
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) continues to infect hundred thousands of people every day worldwide. Since it is a novel virus, research continues to update the possible therapeutic targets when new evidence regarding COVID-19 are gathered. This article presents an evidence-based hypothesis that activating the heme oxygenase-1 (HO-1) pathway is a potential target for COVID-19. Interferons (IFNs) have broad-spectrum antiviral activity including against SARS-CoV-2. Induction of HO-1 and increase in the heme catabolism end-product confer antiviral activity. IFN activation results in inhibition of viral replication in various viral infections. COVID-19 induced inflammation as well as acute respiratory distress syndrome (ARDS), and coagulopathies are now known major causes of mortality. A protective role of HO-1 induction in inflammation, inflammation-induced coagulation, and ARDS has been reported. Based on an association of HO-1 promoter polymorphisms and disease severity, we propose an evaluation of the status of these polymorphisms in COVID-19 patients who become severely ill. If an association is established, it might be helpful in identifying patients at high risk. Hence, we hypothesize that HO-1 pathway activation could be a therapeutic strategy against COVID-19 and associated complications.
引用
收藏
页码:263 / 271
页数:9
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