Key result
Genetically predicted higher kynurenine linked to ~44% higher risk of myocarditis.
Why the study?
The relationship between relevant blood metabolites and the risk of myocarditis has not been well-established.
Do genetically predicted levels of specific human blood metabolites affect the risk of myocarditis in European populations?
Do genetically predicted levels of specific human blood metabolites affect the risk of myocarditis in European populations?
Odds Ratio: 1.441 (95% CI 1.089–1.906)
p-value: p=0.018
Mendelian randomization analysis reveals that genetically predicted higher circulating levels of kynurenine and 1-stearoyl-GPE (18:0) increase the risk of myocarditis, whereas deoxycarnitine and caffeine metabolites may be protective.
Kynurenine and related metabolites may serve as candidate biomarkers; hypothesis-generating for myocarditis risk and leaves open therapeutic targeting.
Myocarditis is a common disease of the cardiovascular and immune systems, but the relationship between relevant blood metabolites and the risk of myocarditis has not been well-established. To identify potential biometabolic markers associated with myocarditis, we conducted a two-sample Mendelian randomization (MR) study. We performed preliminary MR analysis using the inverse variance weighted (IVW) method, supplemented by MR-Egger, weighted median, and weighted mode methods to adjust for false discovery rate (FDR). Confounders were screened using the GWAS Catalog website. Sensitivity analyses included Cochrane Q-test, Egger regression, Mendelian Randomization Pleiotropy RESidual Sum and Outlier (MR-PRESSO), scatterplots, funnel plots, and forest plots. For genetic and directional analysis, we employed co-localization analysis and the Steiger test. MR analysis was performed using the FinnGen database and meta-analysis was performed using the IEU database. MR analysis identified significant correlations for five metabolic biomarkers after FDR correction. These included four known metabolites: kynurenine, 1-stearoyl-GPE (18:0), deoxycarnitine, and 5-acetylamino-6-formylamino-3-methyluracil, as well as one unknown metabolite, X-25,422. Among these, kynurenine (OR = 1.441, 95%CI = 1.089-1.906, p-value = 0.018) and 1-stearoyl-GPE (18:0) (OR = 1.263, 95%CI = 1.029-1.550, p-value = 0.029) were identified as risk factors for myocarditis, while deoxycarnitine (OR = 0.813, 95%CI = 0.676-0.979, p-value = 0.029), 5-acetylamino-6-formylamino-3-methyluracil (OR = 0.864, 95% CI = 0.775-0.962, p-value = 0.018), and X-25,422 (OR = 0.721, 95%CI = 0.587-0.886, p-value = 0.009) were found to be protective factors. No evidence of heterogeneity, horizontal pleiotropy, or sensitivity issues was observed, and no shared genetic factors between exposure and outcome were detected. The causality was in the correct direction. Meta-analysis further confirmed the causal relationship between the five metabolites and myocarditis. This study identifies a causal relationship between five circulating metabolites and myocarditis. Kynurenine, 1-stearoyl-GPE (18:0), deoxycarnitine, X-25,422, and 5-acetylamino-6-formylamino-3-methyluracil may serve as potential drug targets for myocarditis, providing a theoretical basis for the prevention, diagnosis, and treatment of the condition.
No takes yet. Share an insight, caveat, or question.
Wang et al. (2024) studied Myocarditis (n=212,306). Blood metabolome (including kynurenine) vs. Genetically predicted lower levels of metabolites was evaluated on Risk of myocarditis (IVW analysis) (OR 1.441, 95% CI 1.089-1.906, p=0.018). Genetically predicted levels of kynurenine were significantly associated with an increased risk of myocarditis (OR 1.441), alongside four other identified causative or protective metabolites.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: