Problems of Pathogenesis and Pathogenetic Therapy of COVID-19 from the Perspective of the General Theory of Pathological Systems (General Pathological Processes)
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Published on: June 6, 2025
Evgenii Gusev1, Alexey Sarapultsev1,2, Desheng Hu3
1Institute of Immunology and Physiology, Ural Branch of the Russian Academy of Science, 620049 Ekaterinburg, Russia.
Insights
COVID-19 highlights inflammation
Area of Science:
- Pathophysiology
- Critical Care Medicine
- Immunology
Background:
- Pro-inflammatory processes extend beyond classical inflammation concepts.
- Systemic inflammation (SI) involves microcirculatory abnormalities, encompassing cytokine release and thrombo-inflammatory syndrome.
- Persistent low-grade systemic inflammation (ChSLGI) is linked to severe COVID-19 outcomes.
Purpose of the Study:
- To review the multifaceted nature of inflammation in critical conditions like COVID-19.
- To explore the pathogenetic role of inflammatory systemic microcirculation.
- To examine factors contributing to systemic alteration and SI development in COVID-19.
Main Methods:
- Literature review focusing on inflammation, microcirculation, and COVID-19.
- Analysis of pathogenetic mechanisms in critical illness.
- Examination of risk factors for severe COVID-19.
Main Results:
- Inflammatory systemic microcirculation is central to critical situations, including COVID-19.
- Metabolic syndrome models are insufficient for understanding ChSLGI.
- Hypoxia, metabolic dysfunction, and receptor roles in SI development are examined.
Conclusions:
- Systemic inflammation, driven by microcirculatory dysfunction, is key in COVID-19.
- Understanding ChSLGI and its risk factors is crucial for managing severe COVID-19.
- Further research into hypoxia, metabolic factors, and receptor pathways is warranted.
Abstract:
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.
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