ArticleJournal of diabetes research2026
Multiomics Integration Prioritizes ZFP36L1 as a Candidate Susceptibility Gene Associated With Inflammatory and Angiogenic Pathways in Diabetic Retinopathy.
Article in Journal of diabetes research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
Abstract
backgroundDiabetic retinopathy (DR) is a prevalent microvascular complication of diabetes and a leading cause of blindness despite available therapies, underscoring the need for novel therapeutic targets.
methodsIntegrated multiomics analysis combining (1) exploratory single-cell RNA sequencing of rat retinal tissues (three DRs vs. two controls), (2) Mendelian randomization (MR) using whole-blood eQTL data and DR GWAS data (14,584 cases vs. 202,082 controls), and (3) supportive RT-qPCR validation in peripheral-blood clinical samples (30 DRs vs. 30 controls).
results(1) Genetic causality was as follows: MR analysis demonstrated ZFP36L1 as a novel DR risk gene (OR = 1.156, 95% CI = 1.054-1.269, p = 0.002), with significant upregulation in patient blood samples (p < 0.0001). (2) Inflammatory regulation was as follows: ZFP36L1 showed strong correlations with proinflammatory markers (TNF-α and IL-6) and immune cell infiltration (parainflammation and Tregs), while negatively correlating with B cells. (3) Pathway mechanisms were as follows: Functional enrichment analyses suggested potential links between ZFP36L1 and NF-κB-related inflammatory signaling as well as TGF-β-related angiogenic pathways. Despite its known VEGF mRNA destabilizing function, we observed a positive ZFP36L1-VEGF correlation (r = 0.180, p < 0.001), an unexpected finding under diabetic conditions.
conclusionsZFP36L1 is a candidate DR susceptibility gene whose genetically regulated expression in blood is associated with DR risk. Retinal single-cell and pathway analyses provide supportive, hypothesis-generating evidence that ZFP36L1 may be linked to inflammatory and angiogenic processes relevant to DR. Further retina-specific and functional studies are required to determine whether ZFP36L1 directly regulates retinal inflammation or angiogenesis in human DR.
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.