ArticleExperimental and therapeutic medicine2021
Association between the levels of CGI-58 and lipoprotein lipase in the placenta of patients with preeclampsia.
Article in Experimental and therapeutic medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers, 1 of them a synthesis that pooled it.
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Who cites it
5 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Association of LEPTIN and other inflammatory markers with preeclampsia: A systematic review.Frontiers in pharmacology · 2022Pooled it
- Maternal causation of early-onset pre-eclampsia: excessive endometrial gland-derived apolipoprotein D induces placental ferroptosis and developmental abnormalities.Journal of biomedical science · 2025Article
- Article
- PPARγ alleviates preeclampsia development by regulating lipid metabolism and ferroptosis.Communications biology · 2024Article
- The lipase cofactor CGI58 controls placental lipolysis.JCI insight · 2023Article
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5 authors.
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Abstract
Preeclampsia is an idiopathic disease of pregnancy, which seriously endangers the life of both the mother and the infant. The pathogenesis of preeclampsia has not been fully elucidated, although it is generally considered to be associated with abnormal lipid metabolism during pregnancy. Comparative gene identification-58 (CGI-58) and lipoprotein lipase (LPL) are involved in the first step of triglyceride hydrolysis and serve an important role in lipid transport in the placenta. The present study aimed therefore to investigate the association between CGI-58 and LPL in the placentas of patients with or without preeclampsia and to evaluate blood lipid levels. The patient cohort was divided into two groups, pregnant women with preeclampsia and normal pregnant women (control). According to biochemical analyses, reverse transcription-quantitative PCR, immunohistochemistry analysis and western blotting, the expression of CGI-58 and LPL in the placenta was detected, the blood lipid levels were evaluated and other clinical data were collected. Compared with the control group, triglycerides (TGs), low density lipoprotein-cholesterol (LDL-C), apolipoprotein B (ApoB) and atherosclerotic index (AI) were significantly higher in the preeclampsia group, whereas high density lipoprotein-cholesterol (HDL-C) and apolipoprotein A (ApoA) were significantly lower (P<0.05). Furthermore, the expression levels of CGI-58 and LPL in the placental tissue of the preeclampsia group was significantly lower than that of the control group (P<0.05). Linear correlation analysis demonstrated that there was a positive association between CGI-58 and LPL (r=0.602; P<0.05), that CGI-58 was positively associated with HDL-C (r=0.63; P<0.01) but negatively associated with TG and ApoB (r=0.840; P<0.01; and r=0.514; P<0.05, respectively), that LPL was positively associated with HDL-C (r=0.524; P<0.01) but negatively associated with TG and AI (r=0.659; P<0.01; and r=0.496; P<0.01, respectively). These results suggested that the expression of CGI-58 and LPL in the placenta was associated with the pathogenesis of preeclampsia and maternal lipids and the risk of preeclampsia was increased with decreasing expression levels of CGI-58 and LPL. Hence, CGI-58 and LPL may be used as important indicators for the diagnosis of preeclampsia and for the prevention of preeclampsia in pregnant women.
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