Abstract
Human COVID-19 has affected more than 491 million people worldwide. It has caused over 6.1 million deaths and has especially perpetrated a high number of casualties among the elderly and those with comorbid illnesses. COVID-19 triggers a pro-oxidant response, leading to the production of reactive oxygen species (ROS) as a common innate defense mechanism. However, ROS are regulated by a key enzyme called G6PD via the production of reduced nicotinamide adenine dinucleotide phosphate (NADPH), which controls the generation and removal of ROS in a tissue-specific manner. Therefore, a deficiency of G6PD can lead to the dysregulation of ROS, which causes a severe inflammatory response in COVID-19 patients. This report highlights the G6PD dichotomy in the regulation of ROS and inflammatory responses, as well as its deficiency in severity among COVID-19 patients.
Keywords: COVID-19; G6PD deficiency; genetic factor; inflammation; oxidative stress.
【저자키워드】 COVID-19, Inflammation, oxidative stress., G6PD deficiency, genetic factor, 【초록키워드】 Inflammatory responses, severity, Human, Genetic, oxygen, nicotinamide, oxidative stress, G6PD, Control, death, ROS, mechanism, reactive oxygen species, COVID-19 patients, Inflammatory response, genetic factor, Trigger, adenine, dysregulation, phosphate, deficiency, nicotinamide adenine dinucleotide, Regulation, Nicotinamide adenine dinucleotide phosphate, defense mechanism, enzyme, removal, NADPH, illnesses, Defense, highlight, affected, caused, reduced, cause, regulated, reactive oxygen specy, 【제목키워드】 severity of COVID-19, functional, contributing to,