COVID-19, Blood Lipid Changes, and Thrombosis

• Published in: Biomedicines Vol. 11; no. 4; p. 1181
• Main Authors: Farooqui, Akhlaq A, Farooqui, Tahira, Sun, Grace Y, Lin, Teng-Nan, Teh, Daniel B L, Ong, Wei-Yi
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.04.2023; MDPI
• Subjects: Arachidonic acid; autotaxin; Blood; Blood lipids; Blood platelets; Blood vessels; Cell membranes; Clotting; Coronaviruses; COVID-19; Cytokine storm; Eicosanoids; Endothelial cells; Erythrocytes; Genomes; Health aspects; Infections; Inflammation; Leukocytes (neutrophilic); Lipid metabolism; Lungs; Lysophosphatidic acid; Lysophosphatidylcholine; lysophospholipase D; Medical prognosis; Neutrophils; Oxidative stress; Pathogenesis; Phospholipase A2; Phospholipids; PLA2G2A; Platelet-activating factor; Platelets; Prostaglandin H2; Proteins; Review; secretory phospholipase A2; Severe acute respiratory syndrome coronavirus 2; sPLA2-IIA; Thrombosis; Thromboxane A2; Tumor necrosis factor-TNF; Viral infections; Virulence; China; sPLA2-IIA; neutrophil extracellular traps; CAC; macrothrombi; autotaxin; PLA2G2A; microthrombi; C16:0 ceramide; brain endothelial cells; secretory phospholipase A2; stroke; platelets; COVID-19-associated-coagulopathy; COVID-19; NETs; lysophosphatidic acid; thrombosis; lysophospholipase D; LPA; pneumocytes
• ISSN: 2227-9059; 2227-9059
• DOI: 10.3390/biomedicines11041181

Although there is increasing evidence that oxidative stress and inflammation induced by COVID-19 may contribute to increased risk and severity of thromboses, the underlying mechanism(s) remain to be understood. The purpose of this review is to highlight the role of blood lipids in association with thrombosis events observed in COVID-19 patients. Among different types of phospholipases A that target cell membrane phospholipids, there is increasing focus on the inflammatory secretory phospholipase A IIA (sPLA -IIA), which is associated with the severity of COVID-19. Analysis indicates increased sPLA -IIA levels together with eicosanoids in the sera of COVID patients. sPLA could metabolise phospholipids in platelets, erythrocytes, and endothelial cells to produce arachidonic acid (ARA) and lysophospholipids. Arachidonic acid in platelets is metabolised to prostaglandin H2 and thromboxane A , known for their pro-coagulation and vasoconstrictive properties. Lysophospholipids, such as lysophosphatidylcholine, could be metabolised by autotaxin (ATX) and further converted to lysophosphatidic acid (LPA). Increased ATX has been found in the serum of patients with COVID-19, and LPA has recently been found to induce NETosis, a clotting mechanism triggered by the release of extracellular fibres from neutrophils and a key feature of the COVID-19 hypercoagulable state. PLA2 could also catalyse the formation of platelet activating factor (PAF) from membrane ether phospholipids. Many of the above lipid mediators are increased in the blood of patients with COVID-19. Together, findings from analyses of blood lipids in COVID-19 patients suggest an important role for metabolites of sPLA -IIA in COVID-19-associated coagulopathy (CAC).