ArticleJournal of translational medicine2026
Senescence-induced endothelial-to-mesenchymal transition accelerates the subretinal fibrosis in neovascualr age-related macular degeneration.
Article in Journal of translational medicine, 2026. 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
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
1 citing paper in PubMed.
- Cellular crosstalk between endothelial and vascular smooth muscle cells via the BACH1/COL3A1 axis promotes vascular calcification in chronic kidney disease.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 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
13 authors.
Funding
Abstract
backgroundSubretinal fibrosis remains the severe vision loss in neovascular age-related macular degeneration (nAMD), yet effective treatments are still deficient. Cellular senescence and endothelial-to-mesenchymal transition (EndMT) have been implicated in nAMD pathogenesis.
methodsWe analyzed single-cell RNA sequencing data to investigate the role of senescent choriocapillary endothelial cells (CapECs) in subretinal fibrosis. In vitro assays were performed to validate the link between senescence and EndMT. We utilized Brown-Norway rats and INK-ATTAC mice with laser-induced subretinal fibrosis to evaluate the therapeutic effects of senolytic treatment (dasatinib plus quercetin, D + Q) or selective clearance of p16
resultsOur results revealed that CapECs in nAMD exhibited elevated SenMayo gene set variation analysis (GSVA) scores, and upregulated differentially expressed genes (DEGs) were enriched in senescence and mesenchymal transition pathways. A higher proportion of senescence-like CapECs (17.68%) was observed in nAMD, which also showed increased mesenchymal scores and TGFB1 expression. Senescent endothelial cells in laser-induced fibrotic models and bleomycin/doxorubicin-treated human umbilical vein endothelial cells underwent enhanced EndMT. Early intervention with D + Q or removal of p16
conclusionsThe accumulation of senescent endothelial cells promotes subretinal fibrosis via EndMT in nAMD. Targeting these cells represents a promising therapeutic strategy for mitigating fibrosis-associated vision loss.
Indexed as
Identifiers
What OpenQuestion holds
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.