SynthesisArchives of dermatological research2025
Angiostatin: a promising therapeutic target for atopic dermatitis.
Synthesis in Archives of dermatological research, 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.
- Mendelian randomization studies in atopic dermatitis: causal insights across omics layers.Frontiers in immunology · 2026Review
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Angiostatin, a 38-45 KDa proteolytic fragment derived from plasminogen, has garnered significant attention for its dual roles in inhibiting angiogenesis and modulating inflammation. We employed bidirectional Mendelian randomization (MR), meta-analysis, and colocalization to investigate the causal relationship between angiostatin and atopic dermatitis (AD) using three angiostatin and two AD datasets. Additionally, we analyzed global epidemiological trends (1990-2021) and performed transcriptomic profiling of AD. MR analyses revealed a protective effect of angiostatin on AD risk (combined odds ratio: 0.9437, 95% confidence interval [CI]: 0.9198-0.9683, p < 0.0001), while reverse analyses showed no association (standardized mean difference: -0.0029, 95% CI: -0.0516-0.0459, p = 0.9084). Colocalization indicated no shared causal variants (H4 probabilities < 80%). Epidemiological trends highlighted declining age-standardized AD rates despite rising case numbers. Transcriptomic analyses implicated NF-κB, PI3K-Akt, and JAK-STAT pathways in AD pathogenesis. These findings position angiostatin as a dual-action therapeutic candidate, offering novel opportunities to simultaneously target vascular remodeling and immune dysregulation in AD. Translational research is warranted to harness its clinical potential.
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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.