ArticlePeerJ2024
ALKBH5 modulation of ferroptosis in recurrent miscarriage: implications in cytotrophoblast dysfunction.
Article in PeerJ, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- The β-hCG-TNF-α-T cell axis in threatened abortion: unraveling the pathogenic cascade from aberrant glycosylation to inflammatory demise.Frontiers in immunology · 2026Review
- Epigenetics of maternal-fetal interface immune microenvironment and placental related pregnancy complications.Frontiers in immunology · 2025Review
- Ferroptosis and recurrent miscarriage: a critical review of pathophysiology and emerging therapeutic targets.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: As one of the most common and abundant internal modifications of eukaryotic mRNA, N Methods: Recurrent miscarriage (RM) was selected as the main gestational disease in this study. Published data (GSE76862) were used to analyze the gene expression profiles in patients with RM. The extent of m Results: Total m Conclusion: Elevated ALKBH5 alleviated RSL3-induced cytotrophoblast cell death by promoting the expression of FTL in patients with RM. Our results supported the view that ALKBH5 is an important regulator of the ferroptosis-related etiology of RM and suggested that ALKBH5 could be responsible for epigenetic aberrations in RM pathogenesis.
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Registered trials
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