COVID-19, Blood Lipid Changes, and Thrombosis

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 t...

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Published inBiomedicines 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
LanguageEnglish
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
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Abstract 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).
AbstractList 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 A2 that target cell membrane phospholipids, there is increasing focus on the inflammatory secretory phospholipase A2 IIA (sPLA2-IIA), which is associated with the severity of COVID-19. Analysis indicates increased sPLA2-IIA levels together with eicosanoids in the sera of COVID patients. sPLA2 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 A2, 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 sPLA2-IIA in COVID-19-associated coagulopathy (CAC).
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[sub.2] that target cell membrane phospholipids, there is increasing focus on the inflammatory secretory phospholipase A[sub.2] IIA (sPLA[sub.2] -IIA), which is associated with the severity of COVID-19. Analysis indicates increased sPLA[sub.2] -IIA levels together with eicosanoids in the sera of COVID patients. sPLA[sub.2] 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[sub.2] , 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[sub.2] -IIA in COVID-19-associated coagulopathy (CAC).
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 2 that target cell membrane phospholipids, there is increasing focus on the inflammatory secretory phospholipase A 2 IIA (sPLA 2 -IIA), which is associated with the severity of COVID-19. Analysis indicates increased sPLA 2 -IIA levels together with eicosanoids in the sera of COVID patients. sPLA 2 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 2 , 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 2 -IIA in COVID-19-associated coagulopathy (CAC).
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).
Audience Academic
Author Farooqui, Tahira
Farooqui, Akhlaq A
Teh, Daniel B L
Ong, Wei-Yi
Sun, Grace Y
Lin, Teng-Nan
AuthorAffiliation 4 Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119260, Singapore
1 Department of Molecular and Cellular Biochemistry, Ohio State University, Columbus, OH 43210, USA
5 Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119260, Singapore
6 Neurobiology Research Programme, Life Sciences Institute, National University of Singapore, Singapore 119260, Singapore
2 Department of Biochemistry, University of Missouri, Columbia, MO 65211, USA
3 Institute of Biomedical Sciences, Academia Sinica, Taipei 11929, Taiwan
AuthorAffiliation_xml – name: 2 Department of Biochemistry, University of Missouri, Columbia, MO 65211, USA
– name: 1 Department of Molecular and Cellular Biochemistry, Ohio State University, Columbus, OH 43210, USA
– name: 3 Institute of Biomedical Sciences, Academia Sinica, Taipei 11929, Taiwan
– name: 6 Neurobiology Research Programme, Life Sciences Institute, National University of Singapore, Singapore 119260, Singapore
– name: 4 Department of Ophthalmology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119260, Singapore
– name: 5 Department of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 119260, Singapore
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  givenname: Grace Y
  surname: Sun
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/37189799$$D View this record in MEDLINE/PubMed
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Issue 4
Keywords 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
Language English
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Snippet Although there is increasing evidence that oxidative stress and inflammation induced by COVID-19 may contribute to increased risk and severity of thromboses,...
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SubjectTerms 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
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Title COVID-19, Blood Lipid Changes, and Thrombosis
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Volume 11
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