ReviewFrontiers in genetics2025
Exploring the role and therapeutic potential of RNA N6-methyladenosine modification in abortion disease pathology: a comprehensive review.
Review in Frontiers in genetics, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- MAFF promotes decidual stromal cell senescence by suppressing NRF2-mediated antioxidant responses in recurrent pregnancy loss.Journal of assisted reproduction and genetics · 2026Article
Corrections and comments
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recurrent spontaneous abortion (RSA), defined as two or more consecutive pregnancy losses, affects 1%-5% of couples and poses a significant challenge to reproductive health. Despite its prevalence, the underlying etiology remains elusive in approximately half of all cases, hindering the development of targeted therapies. The emerging field of epitranscriptomics, particularly the dynamic and reversible N6-methyladenosine (m6A) RNA modification, offers a novel lens through which to investigate the complex gene-environment interactions underlying RSA. This review systematically synthesizes current knowledge on the pivotal roles of m6A modification in key processes essential for a successful pregnancy: gametogenesis and early embryo quality, placental development and function, and the establishment of immune tolerance at the maternal-fetal interface. We critically evaluate the direct and indirect evidence linking dysregulation of specific m6A regulators to the pathophysiology of RSA, drawing from human tissue studies, RSA animal models, and insights extrapolated from related fields.Furthermore, we discuss the translational potential and considerable challenges of targeting the m6A machinery for therapeutic intervention in RSA. This review aims not only to summarize the current landscape but also to provide a critical framework to guide future mechanistic and clinical research in this promising area.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.