ReviewThe ocular surface2026
A comprehensive review of tear fluid proteome alterations in dry eye disease: Insights into pathophysiology and biomarker potential.
Review in The ocular surface, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
4 citing papers in PubMed.
- Article
- Review
- Association of IL-8 and IL-18 Expression With Histone-Associated NETosis in Aqueous-Deficient and Evaporative Dry Eye Disease.Investigative ophthalmology & visual science · 2026Article
- Serum 25-hydroxyvitamin D and tear-film stability in dry eye disease: A case-control correlation study.Bioinformation · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
Tear fluid is a highly specialized and dynamic biofluid composed of proteins, lipids, mucins, and electrolytes that is essential for maintaining ocular surface integrity, immune defense, and tear film stability. Growing evidence from tear proteomic studieshas revealed extensive alterations in protein composition in dry eye disease (DED), reflecting a complex interplay between local ocular surface pathology and systemic inflammatory influences. This review summarizes proteomic findings from 50 published studies to identify tear proteins that are consistently upregulated or downregulated in DED and to interpret their biological relevance in the context of ocular surface homeostasis. Across studies, proteins upregulated in DED tears predominantly reflect activation of acute-phase and inflammatory pathways, including S100A8/A9, ORM1, APOA2, and proinflammatory cytokines, as well as oxidative stress responses and epithelial remodeling processes. In contrast, downregulated proteins include key protective and homeostatic tear components such as lactoferrin, lysozyme, lipocalin-1, lacritin, and secretoglobins, along with proteins involved in immune transport, epithelial structure, and lipid metabolism that are critical for tear film stability. Overall, these proteomic shifts indicate activation of stress and inflammatory pathways that may perpetuate epithelial barrier damage and tear film instability in DED. By integrating proteomic data across diverse methodologies, this review highlights convergent biological pathways underlying DED pathophysiology and suggests the potential of tear-based protein panels as biomarkers for disease stratification, monitoring, and therapeutic targeting.
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Registered trials
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