ArticleDiscover oncology2025
Comprehensive Mendelian randomization analysis of inflammatory networks in diabetic nephropathy and pituitary adenoma: unveiling complex causal relationships.
Article in Discover oncology, 2025. 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
2 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe intricate relationships between inflammatory pathways, diabetic nephropathy, and pituitary adenomas remain poorly understood. This study aimed to comprehensively investigate the causal associations between inflammatory factors, diabetic nephropathy, and pituitary adenoma risk using Mendelian randomization approaches.
methodsWe conducted a systematic Mendelian randomization analysis employing multiple statistical methods including inverse variance weighted (IVW), MR-Egger, and weighted mode approaches. A comprehensive inflammatory factor profile encompassing cytokines, chemokines, growth factors, and immunoregulatory molecules was analyzed. Sensitivity analyses including scatter plots and funnel plots were performed to validate the robustness of causal inferences.
resultsThe panoramic analysis revealed distinct inflammatory signatures associated with disease risk. For pituitary adenomas, Neurotrophin-3 demonstrated significant protective effects (OR = 0.754, 95% CI: 0.583-0.975, P = 0.031), while programmed cell death 1 ligand emerged as a risk factor (OR = 1.320, 95% CI: 1.016-1.714, P = 0.037). Regarding diabetic nephropathy, six inflammatory factors showed significant associations: CX3C-motif chemokine 1 (OR = 0.514, P = 0.049), interleukin-13 (OR = 0.822, P = 0.014), TNF-beta (OR = 0.903, P = 0.011), and TNF-related activation-induced cytokine (OR = 0.905, P = 0.037) exhibited protective effects, whereas macrophage colony-stimulating factor (OR = 1.175, P = 0.026) and matrix metalloproteinase-10 (OR = 1.142, P = 0.030) increased disease risk. Notably, no significant causal relationship was observed between diabetic nephropathy and pituitary adenoma risk across all analytical methods.
conclusionsThis comprehensive Mendelian randomization analysis reveals complex, disease-specific inflammatory networks underlying diabetic nephropathy and pituitary adenoma pathogenesis.
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.