Background: Preeclampsia (PE) is a significant cause of maternal and neonatal morbidity and mortality worldwide. However, the pathogenesis of PE is unclear and reliable early diagnostic methods are still lacking. The purpose of this review is to summarize potential metabolic biomarkers and pathways of PE, which might facilitate risk prediction and clinical diagnosis, and obtain a better understanding of specific metabolic mechanisms of PE. Methods: This review included human metabolomics studies related to PE in the PubMed, Google Scholar, and Web of Science databases from January 2000 to November 2021. The reported metabolic biomarkers were systematically examined and compared. Pathway analysis was conducted through the online software MetaboAnalyst 5.0. Results: Forty-one human studies were included in this systematic review. Several metabolites, such as creatinine, glycine, L-isoleucine, and glucose and biomarkers with consistent trends (decanoylcarnitine, 3-hydroxyisovaleric acid, and octenoylcarnitine), were frequently reported. In addition, eight amino acid metabolism-related, three carbohydrate metabolism-related, one translationrelated and one lipid metabolism-related pathways were identified. These biomarkers and pathways, closely related to renal dysfunction, insulin resistance, lipid metabolism disorder, activated inflammation, and impaired nitric oxide production, were very likely to contribute to the progression of PE. Conclusion:This study summarized several metabolites and metabolic pathways, which may be associated with PE. These highfrequency differential metabolites are promising to be biomarkers of PE for early diagnosis, and the prominent metabolic pathway may provide new insights for the understanding of the pathogenesis of PE.
Fetal growth restriction (FGR) is a common complication of pregnancy and a significant cause of neonatal morbidity and mortality. The adverse effects of FGR can last throughout the entire lifespan and increase the risks of various diseases in adulthood. However, the etiology and pathogenesis of FGR remain unclear. This study comprehensively reviewed metabolomics studies related with FGR in pregnancy to identify potential metabolic biomarkers and pathways. Relevant articles were searched through two online databases (PubMed and Web of Science) from January 2000 to July 2022. The reported metabolites were systematically compared. Pathway analysis was conducted through the online MetaboAnalyst 5.0 software. For humans, a total of 10 neonatal and 14 maternal studies were included in this review. Several amino acids, such as alanine, valine, and isoleucine, were high frequency metabolites in both neonatal and maternal studies. Meanwhile, several pathways were suggested to be involved in the development of FGR, such as arginine biosynthesis, arginine, and proline metabolism, glyoxylate and dicarboxylate metabolism, and alanine, aspartate, and glutamate metabolism. In addition, we also included 8 animal model studies, in which three frequently reported metabolites (glutamine, phenylalanine, and proline) were also present in human studies. In general, this study summarized several metabolites and metabolic pathways which may help us to better understand the underlying metabolic mechanisms of FGR.
Background Intrahepatic cholestasis of pregnancy (ICP) is a severe idiopathic disorder of bile metabolism; however, the etiology and pathogenesis of ICP remain unclear. Aims This study comprehensively reviewed metabolomics studies related to ICP, to help in identifying the pathophysiological changes of ICP and evaluating the potential application of metabolomics in its diagnosis. Methods Relevant articles were searched through 2 online databases (PubMed and Web of Science) from January 2000 to March 2022. The metabolites involved were systematically examined and compared. Pathway analysis was conducted through the online software MetaboAnalyst 5.0. Results A total of 14 papers reporting 212 metabolites were included in this study. There were several highly reported metabolites: bile acids, such as glycocholic acid, taurochenodeoxycholic acid, taurocholic acid, tauroursodeoxycholic acid, and glycochenodeoxycholic acid. Dysregulation of metabolic pathways involved bile acid metabolism and lipid metabolism. Metabolites related to lipid metabolism include phosphatidylcholine, phosphorylcholine, phosphatidylserine, sphingomyelin, and ceramide. Conclusions This study provides a systematic review of metabolomics of ICP and deepens our understanding of the etiology of ICP.
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