ReviewFrontiers in medicine2025
Multidimensional roles of cfDNA fragmentomics in preeclampsia: from placental hypoxia and TLR9 inflammation to clinical risk stratification.
Review in Frontiers in medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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, 1 synthesis or guideline pooled it.
- Epigenetic alterations in preeclampsia: a systematic review of current mechanisms and biomarker potential.Journal of medicine and life · 2026Pooled it
- Is the HLA System Really Involved in Implantation, Pregnancy, or Abortion of the Fetus?: Strengths, Weaknesses, and Controversial Points.American journal of reproductive immunology (New York, N.Y. : 1989) · 2026Review
- Decoding the immunological triad of TLRs, B1 cells, and feto-maternal microchimerism in pre-eclampsia pathogenesis: a narrative review.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cell-free DNA (cfDNA) has emerged as a pivotal biomarker for predicting preeclampsia (PE), a multisystem syndrome characterized by placental hypoperfusion and systemic inflammation. This review synthesizes critical advances in the field, highlighting quantitative alterations in cfDNA, fragmentomic profiles, and placenta-specific methylation patterns (e.g., RASSF1A) that demonstrate significant value for early prediction and severity stratification of PE. Mechanistically, placental hypoxia-induced trophoblast apoptosis (releasing cfDNA), epigenetic dysregulation activating TLR9/NF-κB inflammatory pathways, and oxidative stress-mediated mitochondrial cfDNA fragmentation collectively drive disease progression. In clinical translation, integrating cfDNA with complementary biomarkers enhances predictive performance, though limitations persist regarding preanalytical variability and dynamic gestational changes. Future efforts must advance fragmentomics-integrated multi-omics frameworks for precision prediction, where assay standardization constitutes the fundamental translational bottleneck.
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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.