ArticleEuropean journal of nutrition2025
Integrative proteomic and metabolomic analysis reveals the mechanisms underlying ischemic stroke induced by vitamin B12 deficiency.
Article in European journal of nutrition, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
BACKGROUND AND
objectiveVitamin B12 deficiency is an emerging public health concern increasingly linked to neurological disorders, including ischemic stroke, yet its underlying molecular mechanisms remain poorly understood. This study aimed to elucidate the molecular basis of vitamin B12 deficiency-associated ischemic stroke by integrating serum-based metabolomic and proteomic analyses.
methodsThis study enrolled patients with first-episode acute ischemic stroke, stratified into vitamin B12-deficient (≤ 250 pg/mL) and non-deficient groups, along with age- and sex-matched healthy controls. Serum samples were collected under standardized conditions and analyzed using untargeted metabolomics via ultra-performance liquid chromatography-mass spectrometry (UPLC-MS) and data-independent acquisition (DIA)-based quantitative proteomics. Differential metabolites and proteins were identified using variable importance in projection, fold change, and p value thresholds. Integrated multi-omics analysis was conducted using pathway enrichment, correlation matrices, and protein–protein interaction networks to uncover shared mechanisms.
results. Compared to healthy individuals, stroke patients with low vitamin B12 levels exhibited pronounced disruptions in lipid and amino acid metabolism. Proteomic analysis identified several differentially expressed proteins, including matrix metalloproteinase-2 (MMP-2), angiotensinogen (AGT), apolipoprotein B (APOB), and glutathione peroxidase 3 (GPX3), which are involved in inflammation, vascular function, and oxidative stress. Network analysis highlighted gamma-aminobutyric acid (GABA) as a central molecule potentially linking vitamin B12 deficiency with neurovascular injury. Enriched pathways included estrogen signaling, neuroactive ligand-receptor interaction, lipid metabolism and atherosclerosis, and cAMP signaling.
conclusionThis study provides the first integrative metabolomic and proteomic evidence that vitamin B12 deficiency may contribute to ischemic stroke by altering lipid metabolism, immune responses, and key regulatory pathways. These findings offer novel molecular insights and potential biomarkers for early detection and targeted intervention in vitamin B12 deficiency-related stroke.
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