The COVID-19 pandemic examines not only the state of actual health care but also the state of fundamental medicine in various countries. Pro-inflammatory processes extend far beyond the classical concepts of inflammation. They manifest themselves in a variety of ways, beginning with extreme physiology, then allostasis at low-grade inflammation, and finally the shockogenic phenomenon of “inflammatory systemic microcirculation”. The pathogenetic core of critical situations, including COVID-19, is this phenomenon. Microcirculatory abnormalities, on the other hand, lie at the heart of a specific type of general pathological process known as systemic inflammation (SI). Systemic inflammatory response, cytokine release, cytokine storm, and thrombo-inflammatory syndrome are all terms that refer to different aspects of SI. As a result, the metabolic syndrome model does not adequately reflect the pathophysiology of persistent low-grade systemic inflammation (ChSLGI). Diseases associated with ChSLGI, on the other hand, are risk factors for a severe COVID-19 course. The review examines the role of hypoxia, metabolic dysfunction, scavenger receptors, and pattern-recognition receptors, as well as the processes of the hemophagocytic syndrome, in the systemic alteration and development of SI in COVID-19.
【저자키워드】 SARS-CoV-2, ARDS, Cytokine storm, systemic inflammation, low-grade inflammation, Microcirculation, MODS, general pathological process, receptor scavengers, 【초록키워드】 COVID-19, Inflammation, severe COVID-19, hypoxia, COVID-19 pandemic, risk factor, Health, pathophysiology, receptors, Care, Critical, Inflammatory response, systemic, specific type, scavenger receptors, syndrome, Abnormalities, cytokine release, metabolic dysfunction, hemophagocytic syndrome, allostasis, extreme, Course, classical, variety, low-grade systemic inflammation, 【제목키워드】 COVID-19, problem, theory, System, pathological,