ArticleFrontiers in immunology2024
Causality of genetically proxied immunophenotypes on cardiovascular diseases: a Mendelian randomization study.
Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Causal Association Between Plasma Proteins and Pericarditis: A Mendelian Randomization Study With Therapeutic Target Identification.Mediators of inflammation · 2026Article
- The role of CD40/CD40L signaling in vascular inflammation and aneurysm progression: a systematic review and evidence synthesis.American journal of translational research · 2026Review
- Article
- Causal relationships between immune cell phenotypes and primary glomerular diseases: genetic evidence from bidirectional Mendelian randomization study.Clinical kidney journal · 2025Article
- Elucidating the molecular association and potential mechanisms between psoriasis and atrial fibrillation through biomarker and immune infiltration analysis.Archives of dermatological research · 2025Article
- Integrated bioinformatic analysis reveals the underlying mitochondria-associated endoplasmic reticulum membranes-related biomarkers for atrial fibrillation.Frontiers in physiology · 2025Article
- TNF superfamily molecules in atherosclerosis: mechanistic insights and therapeutic translation.Frontiers in immunology · 2025Review
- Causal effects of systemic inflammatory proteins on Guillain-Barre Syndrome: insights from genome-wide Mendelian randomization, single-cell RNA sequencing analysis, and network pharmacology.Frontiers in immunology · 2024Article
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: Cardiovascular diseases (CVDs) stand as the foremost global cause of mortality, prompting a growing interest in using the potential of immune cells for heart injury treatment. This study aims to assess the causal association between immune cells and CVDs. Methods: A total of 731 immune cells were derived from a previously published genome-wide association study (GWAS), which included approximately 22 million genetic variants among 3,757 individuals of Sardinian ancestry. Genetic associations with atrial fibrillation (AF), heart failure, coronary artery disease, myocardial infarction and stroke were extracted from large-scale GWAS. A two-sample Mendelian randomization (MR) analysis was used to assess the causal association between immune cells and CVDs. Replication MR analysis based on FinnGen dataset and meta-analysis are sequentially conducted to validate causal relationships. Results: Collectively, genetically predicted 4 immune cell traits were associated with AF and 5 immune cell traits were associated with stroke. Increased levels of IgD- CD38dim absolute count were associated with a higher susceptibility to AF, while increased expression of CD14+ CD16+ monocytes, CD62L on CD62L+ myeloid dendritic cells, and CD16 on CD14- CD16+ monocytes were linked to a decreased susceptibility to AF. Additionally, an elevated susceptibility to stroke was linked to an increase in the percentage of CD39+ resting Tregs and heightened CD27 expression on IgD- CD38+ cells. Conversely, a decreased susceptibility to stroke was associated with increased CD40 expression on monocytes, particularly on CD14+ CD16+ and CD14+ CD16- monocytes, with the latter two showing the most compelling evidence. Conclusion: This study identified several immune cell traits that have a causal relationship with CVDs, thus confirming that immune cells play an important role in the pathogenesis of these diseases.
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