ArticleScientific reports2025
Identification and validation of five novel protein targets for type 2 diabetes mellitus.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- Prenatal Chromium Exposure and Gestational Diabetes Mellitus: Integrating Genetic and Epigenetic Regulation of LPCAT1 from a Phospholipid Remodeling Perspective.Biological trace element research · 2026Article
- Properties of Heterochannels Kv(1.1-1.2)International journal of molecular sciences · 2025Article
- Future horizons in diabetes treatment: hypoglycemic activity of [1,2,4]triazino[2,3-Frontiers in endocrinology · 2025Article
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
Despite advances in type 2 diabetes mellitus (T2DM) therapy, challenges remain due to the lack of novel therapeutic targets. We used Mendelian randomization to integrate cis-expression quantitative trait loci data for circulating proteins from the eQTLGen Consortium (31,684 individuals) with T2DM summary statistics from the Integrative Epidemiology Unit Open Genome-Wide Association Studies Project (61,714 cases, 593,952 controls). 42 genes were significantly associated with T2DM. Colocalization analysis revealed that six genes (CLSTN1, KCNJ11, MLX, DLD, RELA, and ULK1) shared common causal variants with T2DM. Among them, CLSTN1 (OR = 0.80, 95% CI: 0.70-0.90), KCNJ11 (OR = 0.66, 95% CI: 0.60-0.73), and MLX (OR = 0.73, 95% CI: 0.65-0.82) were negatively associated with T2DM, while DLD (OR = 1.38, 95% CI: 1.15-1.65), RELA (OR = 1.90, 95% CI: 1.41-2.55), and ULK1 (OR = 1.42, 95% CI: 1.17-1.71) were positively associated with T2DM. A matched case-control study further validated these associations, except for DLD, showing significant downregulation of CLSTN1, KCNJ11, and MLX (P < 0.05) alongside upregulation of RELA and ULK1 (P < 0.05) in T2DM patients. These findings underscore the potential of these proteins as drug targets, warranting further clinical investigation to confirm their therapeutic relevance.
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.