Evidence map›Paper›PMID 41760022›Full record

ArticleMedicine2026

Bidirectional Mendelian randomization analysis of the relationships between blood cell phenotypes, genetic variants, and systemic lupus erythematosus.

Ju Wei, Hu Liang

Abstract read
In one paragraph

Article in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

2 authors.

Ju WeiEmergency Department, Liuzhou Municipal Liutie Central Hospital, Liuzhou, Guangxi, China.ORCID 0009-0003-0706-8083
Hu LiangDepartment of Internal Medicine, The People's Hospital of Laibin, Laibin, Guangxi, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Based on a bidirectional two-sample Mendelian randomization (MR) analysis of 91 blood cell phenotypes and systemic lupus erythematosus (SLE), this study provides genetic evidence for a complex causal interplay between specific immune cell functions and SLE susceptibility. Forward MR analysis identified 4 perturbation responses - involving eosinophils (response to colchicine), neutrophils (response to potassium chloride and lipopolysaccharide), and platelets (response to nigericin) - as causally linked to SLE risk, with 3 increasing and 1 decreasing susceptibility. Reverse MR analysis revealed that genetic liability to SLE influences 5 blood cell perturbation responses, primarily attenuating neutrophil, monocyte, and white blood cell reactivity. These findings suggest that dysregulated functional responses in key immune cells may act as upstream drivers in SLE pathogenesis, while SLE genetic risk also feeds back to alter cellular behavior, highlighting potential biomarkers and therapeutic targets for SLE prevention and treatment.

Indexed as

Blood CellsGenetic VariationLupus Erythematosus, SystemicMendelian Randomization AnalysisGenetic Predisposition to DiseaseHumansNeutrophilsPhenotypeblood cell phenotypescausal relationshipsgenetic variantsMendelian randomizationsystemic lupus erythematosus

Identifiers

PMID41760022
PMCPMC12956214

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.