ArticleGlobal heart2025
Spontaneous Abortion and Myocardial Infarction: A Mendelian Randomization Investigation and Transcriptomic Analysis.
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 2 papers.
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.
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
2 citing papers in PubMed.
- TMCO1 as an Endoplasmic Reticulum Calcium Load-Activated Channel: Mechanisms and Disease Implications.Biomolecules · 2025Review
- Immune-molecular nexus in reproductive disorders: mechanisms linking POI and RSA.Frontiers in genetics · 2025Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: A link has been found between spontaneous abortion (SA) and myocardial infarction (MI). However, there is still a lack of comprehensive knowledge regarding the genetic links and biological mechanisms between SA and MI. An investigation of the causal association between SA and MI, along with the associated signaling networks, was conducted using univariate Mendelian randomization (MR) and transcriptome analysis. Methods: Data from genome-wide association studies (GWAS) for SA and MI were analyzed using the FinnGen consortium database. To assess the causality between SA and MI, various methods were employed including inverse-variance-weighted (IVW), weighted median, simple mode, and weighted mode analyses. Sensitivity analysis was conducted using heterogeneity, pleiotropy, and the Leave-One-Out (LOO) approach. Transcriptomic analysis of the GSE60993 dataset was performed to identify differentially expressed genes (DEGs) associated with single nucleotide polymorphisms (SNPs). Following this, two bioinformatics analyses were carried out. Results: Based on IVW results, SA was found to be causally associated with MI (OR = 1.095, 95%CI 1.012-1.186). Sensitivity analysis was subsequently conducted to validate the robustness of our findings. Through differential analysis, three key genes - GNAQ, ELP3, and TES - were identified as closely linked to processes related to ribosome biogenesis, DNA replication, and congenital immune deficiency. Furthermore, strong correlations were observed with various immunologic gene sets, including the Major Histocompatibility Complex (MHC), immunoactivators, and immunosuppressors. Conclusion: This study reveals a robust causal relationship between SA and MI, highlighting genetic and immunological pathways that could inform future research and therapeutic approaches.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.