Evidence map›Paper›PMID 40269921›Full record

ArticleTrials2025

Bidirectional Mendelian randomization reveals associations between telomere length and autoimmune diseases.

Qin Jiang, Chenxi Yu, Shiben Zhu, Yang Liu, Min Ye

Abstract read
In one paragraph

Article in Trials, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from 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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Qin Jiang *School of Traditional Chinese Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei, 430061, China.
Chenxi Yu *School of Traditional Chinese Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei, 430061, China.
Shiben Zhu *Department of Infectious Diseases, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China.
Yang LiuSchool of Traditional Chinese Medicine, Hubei University of Chinese Medicine, Wuhan, Hubei, 430061, China.
Min YeDepartment of General Affairs, Shenzhen Baoan Women's and Children's Hospital, Shenzhen, Guangdong, 518001, China. yeminsz@outlook.com.ORCID http://orcid.org/0009-0004-4043-9998

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundAutoimmune diseases are a group of complex chronic illnesses that affect multiple organs or body systems. These diseases are characterized by tissue damage, impaired organ function, and increased risk of malignancies, and elevated mortality. Nevertheless, the casual correlation between autoimmune diseases and telomere length remains uncertain.

objectiveOur bidirectional Mendelian randomization analysis was aimed to evaluate the causal association between autoimmune diseases and telomere length.

methodsTo minimize bias, four demographic factors including body mass index (BMI), alcohol consumption, smoking, and income were assessed using two-sample Mendelian randomization analysis. Furthermore, this analysis was conducted to explore the causal relationships between telomere length and autoimmune diseases, including systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), type 1 diabetes (T1D), Graves' disease (GD), and psoriasis using two separate datasets from FinnGen and the UK Biobank.

resultsWhen using inverse variance weighting (IVW) to assess the relationship between four available demographic factors and overall autoimmune diseases, no significant association was found (p > 0.05). However, a significant negative causal effect of telomere length on autoimmune diseases was observed (IVW: OR = 0.906, 95% CI = 0.832-0.986, p = 0.022). Reverse Mendelian randomization analysis revealed no significant correlation. Further analysis using two separate datasets for five common autoimmune diseases confirmed significant negative associations between telomere length and RA (UKB biobank: OR = 0.997, 95% CI 0.994-0.999, p = 0.025; FinnGen: OR = 0.860, 95% CI 0.741-0.998, p = 0.047), GD (UK Biobank: OR = 0.519, 95% CI 0.430-0.625, p < 0.001; FinnGen: OR = 0.623, 95% CI 0.496-0.785, p < 0.001), and psoriasis (UK Biobank: OR = 0.772, 95%CI = 0.642-0.928, p = 0.006; FinnGen: OR = 0.841, 95%CI = 0.727-0.973, p = 0.020). A significant positive association was found for SLE in the UK Biobank (OR = 1.718, 95% CI = 95% CI 1.155-2.558, p = 0.007). Reverse Mendelian randomization analysis identified a significant negative association between telomere length and SLE (UK Biobank: OR = 0.995, 95% CI 0.991-0.998, p = 0.014; FinnGen: OR = 0.988, 95% CI 0.977-0.998, p = 0.029) and psoriasis (FinnGen: OR = 0.992, 95% CI 0.988-0.997, P = 0.005), and a positive association with RA (UK Biobank: OR = 1.988 95% CI 1.056-3.743, p = 0.031).

conclusionsThis Mendelian randomization analysis reveals a significant association between telomere length and autoimmune diseases such as RA, GD, and psoriasis, while a positive relationship was validated with SLE. These findings underscore the need for further investigation to better understand the underlying mechanisms and their potential clinical applications.

Indexed as

Autoimmune DiseasesMendelian Randomization AnalysisTelomereTelomere HomeostasisTelomere ShorteningGenetic Predisposition to DiseaseHumansRisk FactorsAutoimmune diseasesCasual effectGraves’ diseaseGWASMendelian randomizationPsoriasisRheumatoid arthritisSystemic lupus erythematosusTelomere lengthType 1 diabetes

Identifiers

PMID40269921
PMCPMC12016173

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.