ReviewJournal of translational autoimmunity2026
Circulating cell-free DNA as a biomarker in systemic lupus erythematosus: A narrative review.
Review in Journal of translational autoimmunity, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
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Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Systemic lupus erythematosus (SLE) is a multifactorial, clinically heterogenous autoimmune disease. Reliable biomarkers are essential for early diagnosis, disease activity monitoring, flare prediction, and guiding therapeutic decisions. Biomarkers currently used in clinical practice - such as inflammatory markers, complement levels, and anti-double-stranded DNA (anti-dsDNA) antibodies - are valuable but lack sufficient sensitivity and specificity for predicting flares and disease progression. Circulating cell-free DNA (cfDNA) has emerged as a promising biomarker candidate. Objectives: To provide a comprehensive and critical overview of the current state of knowledge regarding cfDNA in relation to SLE, highlighting key findings, methodological advances, pathomechanistic insights, and areas requiring further research. Methods: This narrative review summarizes key findings on cfDNA in SLE based on studies published between 1966 and 2025. Relevant articles were identified through PubMed and Google Scholar using keywords. Studies investigating cfDNA as a biomarker, methodological advances in cfDNA analysis, and key findings regarding the pathomechanistic relationship between cfDNA and SLE were prioritized. Results: CfDNA originates principally from apoptosis, necrosis, and neutrophil extracellular trap (NET) formation. Advances in molecular technologies have enabled detailed characterization of cfDNA concentration, fragmentation patterns, and epigenetic modifications. These features correlate with disease activity and immunological abnormalities in SLE. More recent studies have expanded the scope of nucleic-acid-based biomarkers. Conclusions: Circulating cfDNA and related nucleic-acid biomarkers represent a promising avenue for improving disease monitoring and personalized management in SLE. However, further large-scale studies and methodological standardization are required before these biomarkers can be routinely implemented in clinical practice.
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