ArticleFrontiers in cell and developmental biology2025
Metabolic-immune crosstalk in myocardial infarction: RLF and SMCHD1 identified as causal therapeutic targets via integrated lactylation-MR analysis.
Article in Frontiers in cell and developmental biology, 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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- Integrated bioinformatics and machine learning reveal pan-apoptosis and immune infiltration signatures in diabetic nephropathy.Frontiers in immunology · 2025Article
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Abstract
Background: The diagnosis of Myocardial Infarction (MI) requires the discovery of specific diagnostic biomarkers beyond high-sensitivity cardiac troponins. To identify causal MI-associated genes regulated by lactylation modification and elucidate their roles in metabolic-immune dysregulation. Methods: This multi-omics study combined bioinformatic analyses of human MI datasets (GSE60993/GSE61144/GSE66360) with experimental validation to investigate lactylation-related genes (LRGs). Differential expression analysis (limma, P < 0.05, |log Results: Integrated transcriptomic analysis of three GEO datasets (73 MI patients, 67 controls) identified 571 DEGs. Cross-referencing these DEGs with 2,051 LRGs yielded 56 Lactylation-associated DEGs. MR analysis using 42,699 instrumental SNPs established RLF (AUC = 0.823) and SMCHD1 (AUC = 0.809) as causal risk genes that were significantly elevated in MI patients. Functional enrichment implicated both genes in metabolic dysregulation (nucleotide metabolism, HIF-1/MAPK signaling) and necroptosis. Immune profiling revealed increased monocytes, neutrophils, and activated CD4 Conclusion: This study pioneers the integration of lactylation modification with MR analysis for MI, establishing RLF and SMCHD1 as causal diagnostic biomarkers. Their dual roles in promoting metabolic dysregulation and pro-inflammatory immune infiltration position them as promising therapeutic targets for MI intervention.
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