ArticleCytoJournal2025
Lysine acetyltransferase 5 contributes to diabetic retinopathy by modulating autophagy through epigenetically regulating autophagy-related gene 7.
Article in CytoJournal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper, 1 of them a synthesis that pooled 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.
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, 1 synthesis or guideline pooled it.
- Cross-Study Meta-Analysis of Blood Transcriptomes in Type 2 Diabetes.International journal of molecular sciences · 2025Pooled it
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Objective: Diabetic retinopathy (DR) is a prevalent and serious complication among individuals with diabetes, significantly compromising their visual acuity and overall quality of life. Lysine acetyltransferase 5 (KAT5), an essential catalytic subunit of the nucleosome acetyltransferase of the H4 complex, is implicated in the development of various diseases, including neurological disorders, breast cancer, and lung cancer. However, the function of KAT5 in DR remains poorly understood. This study aims to investigate the influence of KAT5 on autophagy (Atg) during DR. Material and Methods: Experiments were conducted using streptozotocin (STZ)-treated rats to induce diabetes and observe changes in KAT5 expression and its effect on Atg. Retinal tissues and RF/6A cells were utilized to analyze the expression levels of various proteins and their involvement in Atg and apoptosis. KAT5 depletion and Atg7 knockdown were performed to further understand their roles in the process. Results: The eyeballs of STZ-treated rats showed increased expression of KAT5. Depletion of KAT5 attenuated STZ-induced DR injury in rats. The retinal tissues of STZ-treated rats exhibited reduced expression of B-cell lymphoma-2 (Bcl-2) and increased levels of BCL-2-associated X protein and cleaved caspase 3, which could be reversed by KAT5 depletion. STZ treatment induced expression of Beclin-1 and microtubule-associated protein 1 light chain 3B in retinal tissues, and KAT5 knockdown blocked this effect. In monkey retinal choroidal endothelial ( RF/6A) cells, high glucose (HG) treatment decreased 5-ethynyl-2'-deoxyuridine-positivecells and increased terminal deoxynucleotidyl transferase dUTP nick-end labeling-positive cells, which were reversed by KAT5 depletion. KAT5 depletion also attenuated HG-induced apoptosis and Atg in RF/6A cells. Mechanistically, KAT5 depletion reduced histone H3 lysine 27 acetylation and ribonucleic acid ( RNA) polymerase II enrichment on the Atg7 promoter, leading to a decrease in the messenger RNA ( mRNA) and protein expression of Atg7. Atg7 knockdown suppressed Atg in RF/6A cells under HG conditions and reversed the effect of KAT5 depletion on cell apoptosis and Atg. Conclusion: The findings suggest that KAT5 contributes to DR by modulating Atg through epigenetic regulation of Atg7. KAT5 emerges as a valuable target for DR treatment, providing a fresh perspective on the disease's pathogenesis and laying the foundation for the development of potential therapeutic strategies.
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.