Evidence map›Paper›PMID 38586604›Full record

ArticleMolecular vision2024

Central subfield thickness of diabetic macular edema: Correlation with the aqueous humor proteome.

Lasse Jørgensen Cehofski, Kentaro Kojima, Natsuki Kusada, Mathilde Schlippe Hansen, Danson Vasanthan Muttuvelu, Noëlle Bakker, Ingeborg Klaassen, Jakob Grauslund, Henrik Vorum, Bent Honoré

Abstract read
In one paragraph

Article in Molecular vision, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

  1. MAGIC: Study Design and Rationale for the Phase 2 Clinical Trial of Faricimab for Non-Proliferative Diabetic Retinopathy.Ophthalmologica. Journal international d'ophtalmologie. International journal of ophthalmology. Zeitschrift fur Augenheilkunde · 2026
    Trial
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Lasse Jørgensen CehofskiDepartment of Ophthalmology, Odense University Hospital, Odense, Denmark.
Kentaro KojimaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Natsuki KusadaDepartment of Ophthalmology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Mathilde Schlippe HansenDepartment of Ophthalmology, Odense University Hospital, Odense, Denmark.
Danson Vasanthan MuttuveluDepartment of Ophthalmology, Mitoje Aps, Skive, Denmark.
Noëlle BakkerOcular Angiogenesis Group, Department of Ophthalmology, Amsterdam UMC location University of Amsterdam, Amsterdam, The Netherlands.
Ingeborg KlaassenOcular Angiogenesis Group, Department of Ophthalmology, Amsterdam UMC location University of Amsterdam, Amsterdam, The Netherlands.
Jakob GrauslundDepartment of Ophthalmology, Odense University Hospital, Odense, Denmark.
Henrik VorumDepartment of Ophthalmology, Aalborg University Hospital, Aalborg, Denmark.
Bent HonoréDepartment of Clinical Medicine, Aalborg University, Aalborg, Denmark.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Purpose: Diabetic macular edema (DME) is a sight-threatening complication of diabetes. Consequently, studying the proteome of DME may provide novel insights into underlying molecular mechanisms. Methods: In this study, aqueous humor samples from eyes with treatment-naïve clinically significant DME (n = 13) and age-matched controls (n = 11) were compared with label-free liquid chromatography-tandem mass spectrometry. Additional aqueous humor samples from eyes with treatment-naïve DME (n = 15) and controls (n = 8) were obtained for validation by enzyme-linked immunosorbent assay (ELISA). Best-corrected visual acuity (BCVA) was evaluated, and the severity of DME was measured as central subfield thickness (CST) employing optical coherence tomography. Control samples were obtained before cataract surgery. Significantly changed proteins were identified using a permutation-based calculation, with a false discovery rate of 0.05. A human donor eye with DME and a control eye were used for immunofluorescence. Results: A total of 101 proteins were differentially expressed in the DME. Regulated proteins were involved in complement activation, glycolysis, extracellular matrix interaction, and cholesterol metabolism. The highest-fold change was observed for the fibrinogen alpha chain (fold change = 17.8). Complement components C2, C5, and C8, fibronectin, and hepatocyte growth factor-like protein were increased in DME and correlated with best-corrected visual acuity (BCVA). Ceruloplasmin and complement component C8 correlated with central subfield thickness (CST). Hemopexin, plasma kallikrein, monocyte differentiation antigen CD14 (CD14), and lipopolysaccharide-binding protein (LBP) were upregulated in the DME. LBP was correlated with vascular endothelial growth factor. The increased level of LBP in DME was confirmed using ELISA. The proteins involved in desmosomal integrity, including desmocollin-1 and desmoglein-1, were downregulated in DME and correlated negatively with CST. Immunofluorescence confirmed the extravasation of fibrinogen at the retinal level in the DME. Conclusion: Elevated levels of pro-inflammatory proteins, including the complement components LBP and CD14, were observed in DME. DME was associated with the loss of basal membrane proteins, compromised desmosomal integrity, and perturbation of glycolysis.

Indexed as

Diabetes MellitusDiabetic RetinopathyMacular EdemaAngiogenesis InhibitorsAqueous HumorFibrinogenHumansIntravitreal InjectionsProteomeTomography, Optical CoherenceVascular Endothelial Growth Factor AAngiogenesis InhibitorsFibrinogenProteomeVascular Endothelial Growth Factor A

Identifiers

PMID38586604
PMCPMC10994682

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Registered trials

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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.