Evidence map›Paper›PMID 41174273›Full record

ArticleClinical rheumatology2026

Shared genetic architecture and potential comorbid mechanisms between rheumatoid arthritis and idiopathic pulmonary fibrosis.

Minghao Yuan, Yifeng Zhou, Zhenyi Long, Yameng Peng, Sixian Wu, Yi Chen, Fang Peng, Yizhao Zhou, Lei Wang, Hao Yuan

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Article in Clinical rheumatology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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5 · Who and what money

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10 authors.

Minghao YuanDepartment of Orthopedics, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Yifeng ZhouDepartment of Operating, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Zhenyi LongDepartment of Clinical Laboratory, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Yameng PengDepartment of Clinical Laboratory, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Sixian WuDepartment of Clinical Laboratory, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Yi ChenDepartment of Clinical Laboratory, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Fang PengDepartment of Clinical Laboratory, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Yizhao ZhouDepartment of Orthopedics, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China.
Lei WangBig Data Innovation and Entrepreneurship Education Center of Hunan Province, Changsha University, Changsha, 410022, China. wanglei@xtu.edu.cn.
Hao YuanDepartment of Clinical Laboratory, Hunan Provincial People's Hospital, The First Affiliated Hospital of Hunan Normal University, Changsha, 410005, China. yuanhao666@hunnu.edu.cn.ORCID http://orcid.org/0000-0002-4000-4538

Funding

Distinguished Young Scholar Foundation of Hunan Province No.2023JJ60185Distinguished Young Scholar Foundation of Hunan Province No.2024JJ5052Key Laboratory of Hunan Province-"Energy Saving Control and Safety Monitoring of Rail Transportation No. RS2022A14Natural Science Foundation of Changsha Science and Technology Bureau No. kq2403140Natural Science Foundation of Hunan Province 2021JJ304060the Foundation of Changsha Science and Technology Plan Project No. KZD2501157the National Natural Science Foundation of China No.62272064the Natural Science Foundation of Hunan Provincial Department of Science and Technology No. 2025JJ90184This study was supported by the Key Project of Hunan Provincial Health Commission No. C202311000138
6 · The paper itself

Abstract

objectivesRheumatoid arthritis (RA) and idiopathic pulmonary fibrosis (IPF) commonly coexist, notably in RA-associated interstitial lung disease. Despite clinical overlap, their shared genetic underpinnings remain poorly understood.

methodUsing large-scale genome-wide association study (GWAS) data from European populations, we assessed genetic correlations between RA and IPF through linkage disequilibrium score regression (LDSC) and high-definition likelihood (HDL). Pleiotropic SNPs and shared loci were identified via pleiotropic analysis under the composite null hypothesis (PLACO), functional mapping and annotation of genetic associations (FUMA), and Bayesian colocalization. Multi-marker Analysis of GenoMic Annotation (MAGMA) pinpointed pleiotropic genes, followed by functional enrichment, transcription factor, cell-type specificity, and immune cell colocalization analyses.

resultsSignificant positive genetic correlations were identified (LDSC: rg = 0.321, P = 0.002; HDL: rg = 0.67, P = 5.01 × 10

conclusionsOur findings reveal significant genetic correlations and potential shared genetic mechanisms between RA and IPF, identifying pleiotropic genes and loci involved in immune pathways. This provides foundational genetic insights for exploring pathogenesis and targeted therapies in RA-IPF comorbidity. Key Points • The genetic relationship between rheumatoid arthritis (RA) and idiopathic pulmonary fibrosis (IPF) remains poorly understood despite their frequent clinical coexistence. • We applied genome-wide methods, including LDSC, HDL, PLACO, and MAGMA, to explore shared genetic architecture and immune mechanisms. • Our findings highlight potential common immune-regulatory pathways underlying RA-IPF comorbidity, offering new insights into pathogenesis and therapy development.

Indexed as

Arthritis, RheumatoidIdiopathic Pulmonary FibrosisComorbidityGenetic Predisposition to DiseaseGenome-Wide Association StudyHumansLinkage DisequilibriumPolymorphism, Single NucleotideGenetic correlationGenome-wide association studyIdiopathic pulmonary fibrosisPleiotropic lociRheumatoid arthritis

Identifiers

PMID41174273

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