ArticleBMC pregnancy and childbirth2025
High taurocholic acid concentration induces ferroptosis by downregulating FTH1 expression in intrahepatic cholestasis of pregnancy.
Article in BMC pregnancy and childbirth, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Gut microbiota metabolic reprogramming drives the development of metabolic diseases in the host.Gut microbes · 2026Review
- Peptidomics Landscape of Intrahepatic Cholestasis of Pregnancy and its Molecular Mechanism Investigation.Cell biochemistry and biophysics · 2026Article
- Intrahepatic cholestasis of pregnancy and offspring neurodevelopment: bile acid-mediated mechanisms and long-term neurodevelopmental outcomes.Archives of gynecology and obstetrics · 2026Review
- Analyzing the association between ferritin levels and ICP using machine learning algorithms: a retrospective case-control study.Frontiers in medicine · 2026Article
- Yinzhihuang Oral Liquid Alleviates Intrahepatic Cholestasis of Pregnancy: Integrated Bioinformatics and Experimental Mechanistic Insight.Maternal-fetal medicine (Wolters Kluwer Health, Inc.) · 2025Article
- Dysregulated bile acid metabolism drives lipid peroxidation and ferroptosis in NAFLD: therapeutic potential for traditional Chinese medicine.Frontiers in pharmacology · 2025Review
- Intrahepatic cholestasis of pregnancy associated with azathioprine: first quantitative disproportionality analysis using the FDA adverse event reporting system.Journal of pharmacy & pharmaceutical sciences : a publication of the Canadian Society for Pharmaceutical Sciences, Societe canadienne des sciences pharmaceutiques · 2025Article
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8 authors.
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Abstract
backgroundIntrahepatic cholestasis of pregnancy (ICP) is the most common liver disorder associated with pregnancy and is usually diagnosed based on high serum bile acid. However, the pathogenesis of ICP is unclear. Ferroptosis has been reported as an iron-dependent mechanism of cell death. Although the role of Ferritin Heavy Chain 1 (FTH1) in ferroptosis has been extensively studied in various diseases, its mechanism in ICP through ferroptosis is yet to be analyzed.
methodsPlacental tissues from patients with ICP and healthy controls were employed to verify the expression of FTH1. Taurocholic acid (TCA)-induced HTR-8/SVneo cells were established as an in vitro model for ICP, and ferroptosis-related experiments were performed. In particular, HTR-8/SVneo cells with or without overexpressing FTH1 and HTR-8/SVneo cells with or without TCA induction were investigated to explore the relationship between FTH1 and ferroptosis during ICP in vitro, respectively.
resultsFTH1 was significantly downregulated in the ICP group compared with the control group. Furthermore, FTH1 and ferroptosis-related protein levels were downregulated, while the intracellular iron, reactive oxygen species, and lipid peroxidation levels were upregulated in the TCA-induced HTR-8/SVneo cells. In contrast, ferroptosis was inhibited by overexpression of FTH1 in TCA-induced HTR-8/SVneo cells.
conclusionsA high concentration of TCA in HTR-8/SVneo cells decreased the expression of FTH1. Overexpression of FTH1 could prevent cell death from ferroptosis induced by TCA. Thus, inhibiting the downregulation of FTH1 could be a potential therapeutic target for ICP treatment.
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