ArticleInvestigative ophthalmology & visual science2026
METTL16 Inhibits Lens Epithelial Cells Function in Diabetic Cataract via m6A-Modified DKK1-Mediated Wnt/β-Catenin Signaling.
Article in Investigative ophthalmology & visual science, 2026. 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.
- Expression and mechanistic roles of long non-coding RNAs in diabetic cataract: a systematic review and meta-analysis.Biology direct · 2026Pooled 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
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To explore the role of methyltransferase-like protein 16 (METTL16), an N6-methyladenosine (m6A) methyltransferase, in the development and progression of diabetic cataracts (DCs), as its underlying molecular mechanisms remain unknown. Methods: We evaluated m6A methylation levels in total RNA isolated from DC anterior capsule tissue and high glucose (HG)-induced human lens epithelial cells (HLECs) using m6A quantification and dot blot analysis. The expression levels of METTL16 in the anterior capsule tissue were detected using western blot analysis. Methylated RNA immunoprecipitation (MeRIP), RNA stability assays, and other relevant experiments were performed to investigate the regulatory mechanisms of METTL16 on methylation levels in HLECs. Additionally, cellular functions including proliferation, migration, and cell-cycle progression were assessed. Results: The expression level of METTL16 and the level of m6A methylation were highly elevated in the DC anterior capsule tissue and HG-induced HLECs. MeRIP analysis revealed that Dickkopf-1 (DKK1) might act as the target of METTL16 via the Wnt/β-catenin pathway. Notably, the expression of DKK1 increased with the increase in METTL16 expression in HG-induced HLECs. Furthermore, DKK1 expression was negatively correlated with the nuclear translocation of β-catenin, thereby regulating cell proliferation, migration, and cell-cycle progression in HLECs. In addition, HG-induced lens opacity contributes to cataract formation, and treatment with the DKK1 inhibitor WAY-262611 effectively prevented the development of this pathological process. Conclusions: The METTL16-DKK1-Wnt/β-catenin axis inhibits the proliferation, migration, and cell-cycle progression of HG-induced HLECs. These findings provide an epigenetic insight into the pathogenesis of DC.
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.