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Genetic polymorphisms in vasoactive genes and preeclampsia: a meta-analysis
Igor Medica1, Andrej Kastrin, Borut Peterlin
1Division of Medical Genetics, Department of Gynecology and Obstetrics, University Clinical Centre, Ljubljana, Slovenia.
Genetic variations in angiotensinogen and ACE genes are linked to preeclampsia risk. This meta-analysis clarifies associations for specific polymorphisms, aiding in understanding preeclampsia etiology.
Area of Science:
- Genetics
- Obstetrics
- Molecular Biology
Background:
- Preeclampsia is a pregnancy complication with complex etiology.
- Genetic factors are implicated, but associations with specific gene polymorphisms remain controversial.
Purpose of the Study:
- To systematically evaluate the association between polymorphisms in endothelial nitric oxide synthase (eNOS), angiotensinogen (AGT), angiotensin receptor type 1 (AGTR1), and angiotensin-converting enzyme (ACE) genes and preeclampsia risk.
- To conduct a meta-analysis of studies investigating these genetic variations.
Main Methods:
- Systematic literature search of PubMed for case-control studies up to January 2006.
- Meta-analysis of polymorphisms in eNOS (Glu298Asp), AGT (Met235Thr), and ACE (intron 16 insertion-deletion) genes, including studies with >5 analyses.
- Statistical analysis using odds ratios (OR) and confidence intervals (CI) under dominant and recessive genetic models.
Main Results:
- Significant association found between AGT Met235Thr polymorphism and preeclampsia risk (OR 1.65 dominant, OR 1.54 recessive).
- Significant association found between ACE intron 16 insertion-deletion polymorphism and preeclampsia risk under the recessive model (OR 1.51).
- No single polymorphism demonstrated a major effect on preeclampsia risk.
Conclusions:
- The AGT Met235Thr and ACE intron 16 insertion-deletion polymorphisms are associated with an increased risk of preeclampsia.
- These findings contribute to understanding the genetic underpinnings of preeclampsia.
- Further research is needed to elucidate the precise mechanisms and identify major genetic contributors.
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