ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
SUMOylation is a Translatable Target in Hypoxic MNPs Regulating Retinal Vasculopathy.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. 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.
- Aβ1-40 induces venular endothelial cell ferroptosis in cerebral amyloid angiopathy via the ATF3/xCT axis: Insights from single-cell RNA sequencing.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- PIAS1/PIAS4-Mediated SUMOylation of TDP-43 Is Induced by Oxidative Stress.bioRxiv : the preprint server for biology · 2025Article
- SUMOylation is a Translatable Target in Hypoxic MNPs Regulating Retinal Vasculopathy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Role of histone post-translational modifications in atherosclerosis and the therapeutic potential of targeting epigenetic modifiers.Frontiers in cell and developmental biology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors.
Funding
Abstract
Retinal vasculopathies pose a devastating threat to human health. While anti-VEGF therapy situates the first-line treatment for patients, the clinical efficacy is limited by suboptimal response and potential risks raised by long-term high-dosage use. Neurovascular unit uncoupling is recognized as a key mechanism contributing to pathological neovascularization, yet how immune components get involved is less appreciated. Here, it is reported that SUMOylation modulates the pro-angiogenic capacity of macrophage, and inhibition of the SUMO-conjugating enzyme UBC9 synergizes with anti-VEGF therapy in preclinical models. Diabetic human retinal mononuclear phagocytes (MNPs) overexpress UBC9. Genetic ablation of UBC9 in MNPs compromises the crosstalk with endothelial cells by reducing Vegfa splicing isoforms, including Vegf120, Vegf144, Vegf164, and Vegf188. Mechanistically, hypoxia facilitates the SUMOylation of fused in sarcoma (FUS) protein at lysine residues K327 and K502. Mutation of the SUMOylation sites enhances FUS binding to the Vegfa 3'-untranslated region (3'UTR), leading to mRNA destabilization and decreased VEGFA production. Intravitreal administration of anti-VEGF elevates UBC9 whereas Ubc9 siRNA-liposomes alleviates retinal vascular leakage and choroidal neovascularization, and a better therapeutic efficacy is yielded when combining with anti-VEGF therapy. Taken together, this study highlights a novel approach for treating retinal vascular diseases by modulating the MNPs-endothelial cell interplay.
Indexed as
Identifiers
What Socratic 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 Socratic graph.