COVID-19 AND OXIDATIVE STRESS

Pathogenesis of the novel coronavirus infection COVID-19 is the subject of active research around the world. COVID-19 caused by the SARS-CoV-2 is a complex disease in which interaction of the virus with target cells, action of the immune system and the body’s systemic response to these events are closely intertwined. Many respiratory viral infections, including COVID-19, cause death of the infected cells, activation of innate immune response, and secretion of inflammatory cytokines. All these processes are associated with the development of oxidative stress, which makes an important contribution to pathogenesis of the viral infections. This review analyzes information on the oxidative stress associated with the infections caused by SARS-CoV-2 and other respiratory viruses. The review also focuses on involvement of the vascular endothelium in the COVID-19 pathogenesis. Патогенез новой коронавирусной инфекции COVID-19 является предметом активного изучения во всем мире. COVID-19, вызываемый SARS-CoV-2, представляет собой сложное заболевание, в котором тесно переплетено взаимодействие вируса с клетками-мишенями, действием иммунной системы и системной реакцией организма на эти события. Многие респираторные вирусные инфекции, включая COVID-19, вызывают смерть инфицированных клеток, активацию компонентов врожденного иммунитета и секрецию цитокинов воспаления. Все эти процессы ассоциированы с развитием окислительного стресса, который вносит важный вклад в патогенез вирусных инфекций. В данном обзоре проведен анализ информации об окислительном стрессе при инфекциях, вызываемых SARS-CoV-2 и другими респираторными вирусами. Основное внимание в обзоре уделено участию сосудистого эндотелия в патогенезе COVID-19.

COVID-19 and Oxidative Stress.

Pathogenesis of the novel coronavirus infection COVID-19 is the subject of active research around the world. COVID-19 caused by the SARS-CoV-2 is a complex disease in which interaction of the virus with target cells, action of the immune system and the body's systemic response to these events are closely intertwined. Many respiratory viral infections, including COVID-19, cause death of the infected cells, activation of innate immune response, and secretion of inflammatory cytokines. All these processes are associated with the development of oxidative stress, which makes an important contribution to pathogenesis of the viral infections. This review analyzes information on the oxidative stress associated with the infections caused by SARS-CoV-2 and other respiratory viruses. The review also focuses on involvement of the vascular endothelium in the COVID-19 pathogenesis.

NETosis: Molecular Mechanisms, Role in Physiology and Pathology.

NETosis is a program for formation of neutrophil extracellular traps (NETs), which consist of modified chromatin decorated with bactericidal proteins from granules and cytoplasm. Various pathogens, antibodies and immune complexes, cytokines, microcrystals, and other physiological stimuli can cause NETosis. Induction of NETosis depends on reactive oxygen species (ROS), the main source of which is NADPH oxidase. Activation of NADPH oxidase depends on increase in the concentration of Ca2+ in the cytoplasm and in some cases on the generation of ROS in mitochondria. NETosis includes release of the granule components into the cytosol, modification of histones leading to chromatin decondensation, destruction of the nuclear envelope, as well as formation of pores in the plasma membrane. In this review, basic mechanisms of NETosis, as well as its role in the pathogenesis of some diseases including COVID-19 are discussed.

NETosis: MOLECULAR MECHANISMS, ROLE IN PHYSIOLOGY AND PATHOLOGY

NETosis is a program for formation of neutrophil extracellular traps (NETs), which consist of modified chromatin decorated with bactericidal proteins from granules and cytoplasm. Various pathogens, antibodies and immune complexes, cytokines, microcrystals, and other physiological stimuli can cause NETosis. Induction of NETosis depends on reactive oxygen species (ROS), the main source of which is NADPH oxidase. Activation of NADPH oxidase depends on increase in the concentration of Ca²⁺ in the cytoplasm and in some cases on the generation of ROS in mitochondria. NETosis includes release of the granule components into the cytosol, modification of histones leading to chromatin decondensation, destruction of the nuclear envelope, as well as formation of pores in the plasma membrane. In this review, basic mechanisms of NETosis, as well as its role in the pathogenesis of some diseases including COVID-19 are discussed. НЕТоз - это программа образования нейтрофильных внеклеточных ловушек или NET (neutrophil extracellular traps), состоящих из модифицированного хроматина и связанных с ним бактерицидных белков гранул и цитоплазмы. НЕТоз могут вызывать различные патогены, антитела и иммунные комплексы, цитокины, микрокристаллы и другие физиологические стимулы. Индукция НЕТоза зависит от активных форм кислорода (АФК), основным источником которых служит NADPH-оксидаза. Активация NADPH-оксидазы зависит от повышения концентрации Са²⁺ в цитоплазме и в некоторых случаях от генерации АФК в митохондриях. В процессе НЕТоза происходит выход компонентов гранул в цитозоль, модификация гистонов, ведущая к деконденсации хроматина, разрушение ядерной оболочки, а также образование пор в плазматической мембране. В обзоре обсуждаются основные представления о механизмах НЕТоза, а также роль НЕТоза в патогенезе некоторых заболеваний, включая COVID-19.