ArticleRenal failure2025
Exploring the relationship between graft dysfunction with serum metabolites and inflammatory proteins: integrating Mendelian randomization, single-cell analysis, machine learning, and SHAP methods for comprehensive analysis.
Article in Renal failure, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Machine learning-based prediction model and web calculator for postoperative LDVT in colorectal cancer.Frontiers in oncology · 2025Article
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5 authors.
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Abstract
backgroundThe exact mechanism of graft dysfunction has not been fully clarified. We aimed to explore the causal effects of serum metabolites on graft dysfunction and the mediating role of inflammatory proteins.
methodsWe first analyzed the causal association of 1,091 serum metabolites and 91 inflammatory proteins with graft dysfunction by Mendelian randomization (MR) to find the most important indicators and calculated the mediating role of inflammatory proteins. Second, we further intergrated the single-cell analysis, machine learning, and Shapley Additive exPlanations (SHAP) methods to validate the role of the inflammatory protein in rejected transplanted kidneys.
resultsIn MR analysis, the inverse variance weighted (IVW) method showed that N-acetylaspartyl glutamate (NAAG) levels reduced the risk of graft dysfunction (OR 0.648, 95% CI 0.522-0.805). Interleukin-2 receptor subunit beta (IL-2RB) mediated the association between NAAG and graft dysfunction with a mediation ratio of 11.35% (95% CI 1.85%-24.69%). In transplanted kidneys, IL-2RB is predominantly expressed elevated in T cells from rejection samples and is associated with decreased renal function. 10 hub genes were identified based on T cells with high and low expression of IL-2RB, of which NGboost reached AUC 0.77. The SHAP method obtained the gene with the greatest model contribution: the IL-2RB gene.
conclusionNAAG plays a protective role in graft dysfunction, and part of the effect is mediated by inhibition of IL-2RB, which is verified as an important gene that functions in transplant kidney rejection. NAAG and IL-2RB may be novel molecular markers and therapeutic targets for graft dysfunction.
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