ArticleMedicine2025
Causal analysis of 731 immunophenotypes and heart failure: A bidirectional Mendelian randomization study.
Article in Medicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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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.
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.
Who cites it
1 citing paper in PubMed.
- From Tissue to Transcriptome: A Systematic Review of Multi-Level Evidence for Immune Dysregulation in Atrial Fibrillation.Journal of clinical medicine · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
The aim of this study was to elucidate the causal relationship between immunophenotypes and heart failure (HF) using bidirectional Mendelian randomization (MR) analysis. Summary-level data for HF and immunophenotypes were obtained from public genome-wide association study data. Five robust MR methods were employed to delineate the causal effects between the 2. Further analyses included horizontal pleiotropic analysis, Cochran Q analysis, MR-Egger intercept test, and leave-one-out analysis. Finally, we used the screened immunophenotypes as outcomes and HF as exposure for reverse MR analyses. Eight immunophenotypes demonstrated an increased risk of HF, including immunoglobin D+ (IgD+) CD38br absolute cell (AC); double positive (CD4+CD8+) %leukocyte; CD28- CD127- CD25++ CD8br %T cell; CD28- CD127- CD25++ CD8br %CD8br; CD28+ CD45RA+ CD8br %T cell; CD19 on IgD+ CD38br; CD27 on IgD- CD38dim; CD45 on lymphocyte. Conversely, 7 immunophenotypes exhibited a reduced risk of HF, including Activated Treg AC; Im myeloid-derived suppressor cell %CD33dim human leukocyte antigen DR- (HLA DR-) CD66b-; CD33dim HLA DR+ CD11b+ %CD33dim HLA DR+; CD20 on IgD- CD38dim; side scatter-A (SSC-A) on CD14+ monocyte; SSC-A on HLA DR+ natural killer cell; CD11b on CD14+ monocyte. Importantly, we did not find any horizontal multidimensional outliers, genetic heterogeneity, directional pleiotropy, or a single nucleotide polymorphism that determines ultimate causality. The results of the reverse MR analysis were not statistically significant. In this study, the genetic correlation between 15 immunophenotypes and HF was revealed by MR analysis, which provides a reference for future clinical treatment.
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Registered trials
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