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Differential Effects of Lipid-lowering Drugs in Modulating Morphology of Cholesterol Particles
Published on: November 10, 2017
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COVID-19, Blood Lipid Changes, and Thrombosis
Akhlaq A Farooqui1, Tahira Farooqui1, Grace Y Sun2
1Department of Molecular and Cellular Biochemistry, Ohio State University, Columbus, OH 43210, USA.
Biomedicines
|May 16, 2023
Summary
COVID-19 coagulopathy involves blood lipids. Secretory phospholipase A2 IIA (sPLA2-IIA) metabolites, like arachidonic acid and lysophosphatidic acid, promote thrombosis in COVID-19 patients.
Area of Science:
- Biochemistry
- Immunology
- Pathology
Background:
- COVID-19 is linked to increased thrombosis risk and severity.
- Oxidative stress and inflammation are implicated, but mechanisms are unclear.
- Blood lipid alterations are increasingly recognized in COVID-19 patients.
Purpose of the Study:
- To review the role of blood lipids in COVID-19-associated thrombosis.
- To highlight the involvement of secretory phospholipase A2 IIA (sPLA2-IIA) and its metabolites.
Main Methods:
- Review of existing literature on COVID-19, thrombosis, and lipid mediators.
- Analysis of studies reporting sPLA2-IIA, eicosanoids, and other lipid levels in COVID-19 patients.
Main Results:
- Elevated sPLA2-IIA and eicosanoids are found in COVID-19 patients.
- sPLA2-IIA metabolizes phospholipids into pro-coagulant mediators like arachidonic acid and lysophosphatidic acid (LPA).
- Increased autotaxin (ATX) and LPA contribute to NETosis, a key feature of COVID-19 hypercoagulability.
Conclusions:
- Metabolites of sPLA2-IIA play a significant role in COVID-19-associated coagulopathy (CAC).
- Targeting lipid mediator pathways may offer therapeutic strategies for managing COVID-19 complications.
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