ArticleCurrent medicinal chemistry2026
A Bi-directional Mendelian Randomization Study of Idiopathic Pulmonary Fibrosis and Six Diabetes-related Traits.
Article in Current medicinal chemistry, 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
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionThe objective of the present study was to explore the bi-directional causal relationship between IPF and diabetes (type 1 diabetes and type 2 diabetes)/ diabetic nephropathy/glycemic traits [fasting glucose and glycated hemoglobin (HbA1c)]/fasting blood insulin through MR analysis.
methodsA bi-directional two-sample Mendelian randomization (MR) study design was adopted to evaluate the causal relationship between IPF and diabetes (type 1 diabetes and type 2 diabetes), diabetic complications (diabetic nephropathy) and glycemic traits [fasting blood glucose, glycated hemoglobin (HbA1c), fasting insulin] in a European population. Genome-wide association study summary data was obtained. The inverse variance weighted (IVW) method with a fixed-effects model was used to estimate the primary causal effects. The causal effects are represented by reporting odds ratios (OR) and their corresponding 95% confidence intervals (CI). The robustness of results was assessed using the MR-Egger and Weighted Median methods.
resultsIn the forward MR analysis, the IVW method revealed a significant causal effect of IPF on type 2 diabetes (OR=1.031, 95% CI: 1.011-1.052). Similar estimates were obtained through the Weighted Median method. However, no significant causal effects were observed on type 1 diabetes, diabetic nephropathy, fasting blood glucose, HbA1c, and fasting insulin, respectively (p>0.05). We performed the reverse MR analysis using similar methods to the forward MR approach. MR analysis only showed a significant causal association of fasting insulin with IPF risk, with an OR of 3.576 (95% CI: 1.958-6.531). DISCUSSION: Genetically determined IPF was linked to an elevated risk of type 2 diabetes. The inverse MR analysis indicated that there was no causal impact of genetically predicted type 2 diabetes on the IPF risk.
conclusionGenetically predicted fasting blood insulin was found to be positively associated with IPF risk.
Indexed as
Identifiers
41178771What 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.