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Author Spotlight: Modeling an Aspect of Preeclampsia in Female Mice Using Hypoxic Human Placenta-Derived Small Extracellular Vesicles
Published on: January 26, 2024
Possible effects of lipoprotein-associated phospholipase A2 single-nucleotide polymorphisms on cardiovascular risk in
Zeynep B Güngör1, Abdullah Tüten2, Hakan Ekmekçi1
1a Department of Medical Biochemistry , Cerrahpasa Medical School, University of Istanbul , Istanbul , Turkey.
Insights
Lipoprotein lipase-associated phospholipase A2 (Lp-PLA2) levels are elevated in preeclampsia (PE) and linked to future cardiovascular disease (CVD) risk. Genetic variations in PLA2G7 may increase CVD risk in women with PE.
Area of Science:
- Cardiovascular Disease Research
- Reproductive Health and Inflammation
- Genetic Epidemiology
Background:
- Lipoprotein lipase-associated phospholipase A2 (Lp-PLA2) is a key marker of vascular inflammation.
- Preeclampsia (PE) is associated with heightened vascular inflammation and increased long-term cardiovascular disease (CVD) risk in women.
- Genetic factors influencing vascular inflammation may predispose women with PE to future CVD.
Purpose of the Study:
- To investigate the association between PLA2G7 gene polymorphisms, Lp-PLA2 levels, and cardiovascular risk factors in women with preeclampsia.
- To determine if vascular inflammation-related genetic variations increase the risk of developing future cardiovascular disease in women with PE.
Main Methods:
- A study involving 200 pregnant women, stratified into early-onset PE, late-onset PE, and control groups.
- Measurement of serum Lp-PLA2 mass, activity, index, Hs-C-reactive protein (CRP), serum amyloid A (SAA), calprotectin, and PTX3 levels.
- Analysis of PLA2G7 single-nucleotide polymorphisms (SNPs) rs1805017 and rs9381475 for correlation with Lp-PLA2 mass and logistic regression for risk assessment.
Main Results:
- Serum Lp-PLA2 mass was significantly higher in both early and late PE groups compared to controls (p < 0.001).
- Elevated levels of Lp-PLA2 index, Hs-CRP, SAA, calprotectin, and PTX3 were observed in PE groups (p < 0.001).
- PLA2G7 SNPs rs1805017 and rs9381475 showed correlations with Lp-PLA2 mass in the early PE group, with carriers identified as an independent risk factor.
Conclusions:
- Elevated Lp-PLA2 mass and specific PLA2G7 genetic variations are associated with preeclampsia.
- These findings suggest that Lp-PLA2 genetic variability and elevated vascular inflammatory markers may contribute to the incidence of future cardiovascular events in women with a history of PE.
Purpose:
Lipoprotein lipase-associated phospholipase A2 (Lp-PLA2) is a vascular inflammatory marker associated with cardiovascular diseases (CVD). Women with preeclampsia (PE) have elevated vascular inflammation and at higher CVD risk in the later life. We hypothesize that vascular inflammation related genetic variations increase the risk for developing future cardiovascular disease in women with PE. To test this hypothesis, we studied PLA2G7 gene polymorphisms, Lp-PLA2 mass, activity, index, and other cardiovascular risk factors in women with preeclampsia.
Methods:
A total of 200 pregnant women were included into the study. We stratified the PE group: early (28.7 ± 3.0 weeks) and late onset (36.0 ± 1.4 weeks). Serum Lp-PLA2 mass in the early PE and the late PE group were significantly higher than the control group (p = .000). Lp-PLA2 index, Hs-C-reactive protein (CRP), serum amyloid A (SAA), calprotectin, and PTX3 levels were higher in early and late PE (p = .000). Single-nucleotide mutations of PLA2G7 rs1805017 (r = -0.228, p < .05) and rs9381475 (r = 0.216, p < .05) were correlated with LpPLA2 mass for the early PE group. Logistic regression analysis showed that LP-PA2 mass an independent risk factor for early PE with rs1805017 and rs9381475 carriers.
Conclusions:
Lp-PLA2 genetic variability with vascular inflammatory markers might contribute the incidence of future cardiovascular events.
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