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Coronaviruses and stress: from cellular to global
Lawrence E Hightower1, M Gabriella Santoro2,3
1Department of Molecular and Cell Biology, University of Connecticut, Storrs, CT, 06269, USA. lawrence.hightower@uconn.edu.
Cell Stress & Chaperones
|September 5, 2020
Summary
This research explores how SARS-CoV-2 causes COVID-19, focusing on molecular mimicry and vascular endothelial damage. New therapies targeting endothelial protection, including hyperbaric oxygen, are proposed for treating this viral infection.
Area of Science:
- Cellular and Molecular Biology
- Immunology
- Pathophysiology
Background:
- Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) emerged in late 2019, causing the COVID-19 pandemic.
- Researchers observed parallels between COVID-19 pathophysiology and cell stress responses studied independently.
- This special issue focuses on the cell stress response field's insights into COVID-19.
Discussion:
- Molecular mimicry between viral proteins and host proteins is a key theme.
- Immune mimicry may lead to autoimmune-induced vascular endothelial damage in multiple organs.
- Therapeutic strategies focus on protecting the vascular endothelium.
Key Insights:
- Identified molecular mimicry as a significant factor in COVID-19.
- Highlighted the role of vascular endothelial cells in COVID-19 pathogenesis.
- Proposed novel therapeutic targets for endothelial protection.
Outlook:
- Investigated chemical treatments like stannous chloride and hydrogen sulfide inducers.
- Explored heme oxygenase inducers for cytoprotective effects.
- Advanced hyperbaric oxygen therapy as a potential treatment for COVID-19 by activating cellular defense systems.
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