ArticleGlobal heart2025
Exploring the Causal Link Between Autoimmune Diseases and Pulmonary Arterial Hypertension: A Bidirectional Mendelian Randomization Study.
Article in Global heart, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
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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.
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Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Causal risk and protective factors for rheumatoid arthritis: a comprehensive mendelian randomization systematic review and meta-analysis.Frontiers in genetics · 2026Pooled it
- The causal relationship between diabetes mellitus and hashimoto thyroiditis: A two-sample mendelian randomization analysis.Medicine · 2026Article
- Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Pulmonary arterial hypertension (PAH) is a severe vascular disorder with a multifactorial etiology, including potential genetic predispositions. Understanding the causal relationship between autoimmune diseases and the risk of developing PAH can inform clinical strategies for prevention and treatment. Methods: We conducted a two-sample Mendelian Randomization (MR) analysis to evaluate the causal effect of genetic predisposition to five autoimmune diseases (systemic lupus erythematosus [SLE], rheumatoid arthritis [RA], inflammatory bowel disease [IBD], multiple sclerosis [MS], and type 1 diabetes [T1D]) on the risk of PAH. This involved employing various MR methods (IVW, MR-Egger, Weighted median, Simple mode, and Weighted mode), as well as conducting tests for heterogeneity and horizontal pleiotropy. Results: The analysis revealed a significant association between genetic predisposition to RA and IBD with an increased risk of PAH (RA: OR = 1.28, 95% CI [1.01-1.61], p = 0.042; IBD: OR = 1.29, 95% CI [1.01-1.64], p = 0.043). However, no association was observed between genetically determined MS, SLE, and T1D with the risk of PAH (MS: p = 0.876; SLE: p = 0.564; T1D: p = 0.061). Additionally, tests for heterogeneity and pleiotropy provided no evidence of their influence, suggesting the robustness of these associations. Reverse MR analysis also indicated no significant effect of PAH on the genetic susceptibility to these autoimmune diseases. Conclusion: The findings suggest a possible genetic causative link between RA and IBD and the risk of developing PAH. Conversely, genetic predisposition to MS, SLE, and T1D does not appear to influence PAH risk. Understanding these relationships may offer insights into the pathophysiology of PAH and inform screening strategies within at-risk populations.
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