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Background <p>Placenta accreta spectrum (PAS) is a serious obstetric complication with limited understanding of its molecular basis. This study investigates metabolic and transcriptomic alterations in PAS placentas to uncover potential mechanisms and biomarkers.</p> Methods <p>Placental tissues from PAS patients (<i>n</i> = 19) and controls (<i>n</i> = 10) underwent untargeted metabolomics via Liquid chromatography–tandem mass spectrometry (LC-MS/MS). Differential metabolites were analyzed for pathway enrichment. RNA sequencing was performed to identify differentially expressed genes (DEGs), followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) and disease ontology enrichment. Integrated metabolomic-transcriptomic analysis was used to identify key metabolic pathways, and findings were validated in an expanded cohort (22 PAS cases, 50 controls). Receiver operating characteristic (ROC) curve analysis was performed to assess the diagnostic performance of Lecithin, phosphate cytidylyltransferase 1 beta (PCYT1B), and their combination for predicting PAS.</p> Results <p>A total of 203 metabolites were differentially expressed in PAS placentas, with lipid and lipid-like molecules comprising the largest class. Several phosphatidylcholine (PC) species were significantly upregulated, indicating dysregulated glycerophospholipid metabolism. Transcriptome analysis identified 578 DEGs, including upregulation of PCYT1B and endothelial lipase (LIPG), both involved in lipid metabolism. Enrichment analysis revealed activation of glycerolipid and glycosphingolipid pathways and the potential involvement with metabolic disorders. Integrated analysis highlighted enhanced phosphatidylcholine biosynthesis, supported by elevated PCYT1B expression and increased total PC levels in PAS placentas. Lecithin showed higher sensitivity but lower specificity, while PCYT1B displayed intermediate performance. Their combination yielded the best discrimination with an area under the curve (AUC) of 0.791 (95% CI: 0.684–0.899).</p> Conclusions <p>PAS is characterized by significant alterations in lipid metabolism, particularly increased phosphatidylcholine biosynthesis via the Kennedy pathway. These findings provide new insights into the molecular pathogenesis of PAS and suggest potential metabolic targets for early diagnosis or intervention.</p>

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Integrated metabolomic and transcriptomic analysis identifies enhanced phosphatidylcholine metabolism in placenta accreta spectrum

  • 期刊论文

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  • 发表日期：

    2026年6月23日

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  • Zhenping Liu,
  • Xijiang Liu,
  • Wenxia Zhang,
  • Chenggong Sun,
  • Yuyan Ma,
  • Hongyan Wang

摘要

Background

Placenta accreta spectrum (PAS) is a serious obstetric complication with limited understanding of its molecular basis. This study investigates metabolic and transcriptomic alterations in PAS placentas to uncover potential mechanisms and biomarkers.

Methods

Placental tissues from PAS patients (n = 19) and controls (n = 10) underwent untargeted metabolomics via Liquid chromatography–tandem mass spectrometry (LC-MS/MS). Differential metabolites were analyzed for pathway enrichment. RNA sequencing was performed to identify differentially expressed genes (DEGs), followed by Kyoto Encyclopedia of Genes and Genomes (KEGG) and disease ontology enrichment. Integrated metabolomic-transcriptomic analysis was used to identify key metabolic pathways, and findings were validated in an expanded cohort (22 PAS cases, 50 controls). Receiver operating characteristic (ROC) curve analysis was performed to assess the diagnostic performance of Lecithin, phosphate cytidylyltransferase 1 beta (PCYT1B), and their combination for predicting PAS.

Results

A total of 203 metabolites were differentially expressed in PAS placentas, with lipid and lipid-like molecules comprising the largest class. Several phosphatidylcholine (PC) species were significantly upregulated, indicating dysregulated glycerophospholipid metabolism. Transcriptome analysis identified 578 DEGs, including upregulation of PCYT1B and endothelial lipase (LIPG), both involved in lipid metabolism. Enrichment analysis revealed activation of glycerolipid and glycosphingolipid pathways and the potential involvement with metabolic disorders. Integrated analysis highlighted enhanced phosphatidylcholine biosynthesis, supported by elevated PCYT1B expression and increased total PC levels in PAS placentas. Lecithin showed higher sensitivity but lower specificity, while PCYT1B displayed intermediate performance. Their combination yielded the best discrimination with an area under the curve (AUC) of 0.791 (95% CI: 0.684–0.899).

Conclusions

PAS is characterized by significant alterations in lipid metabolism, particularly increased phosphatidylcholine biosynthesis via the Kennedy pathway. These findings provide new insights into the molecular pathogenesis of PAS and suggest potential metabolic targets for early diagnosis or intervention.