Reactive oxygen species, proinflammatory and immunosuppressive mediators induced in COVID-19: overlapping biology with cancer†

Abstract

This review analyzes the published literature linking the different mechanisms focused on oxidative stress and inflammation that contribute to COVID-19 disease severity. The objective is to bring together potential proinflammatory mechanisms of COVID-19 pathogenesis and address mitigation strategies using naturally occurring compounds and FDA-approved drugs. Outstanding questions addressed include the following: What is the mechanistic basis for linking enhanced vulnerability in COVID-19 to increased oxidative damage and proinflammatory mediators ( e.g., cytokines), especially in high-risk people? Can we repurpose anti-inflammatory and immunomodulatory agents to mitigate inflammation in COVID-19 patients? How does 2-deoxy- d-glucose function as an anti-COVID drug? COVID-19, cancer biology, and immunotherapy share many mechanistic similarities. Repurposing drugs that already have been FDA-approved for mitigating inflammation and immunosuppression in cancer may be a way to counteract disease severity, progression, and chronic inflammation in COVID-19. What are the long-term effects of reactive oxygen species-inducing immune cells and sustained inflammation in so-called long-haulers (long COVID) after recovery from COVID-19? Can we use mitochondria-targeted agents prophylactically to prevent inflammation and boost immunity in long-haulers? Addressing the oxidative chemical biology of COVID-19 and the mechanistic commonalities with cancer may provide new insights potentially leading to appropriate clinical trials and new treatments.

Abstract

Mitochondria-targeted drugs inhibit cancer and COVID-19 mechanisms.