ArticlePediatric research2026
Mechanisms of lactylation-related biomarker in neonatal hypoxic-ischemic brain damage analyzed through multi-omics data.
Article in Pediatric research, 2026. 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.
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundNeonatal hypoxic-ischemic brain damage (HIBD) treatment is challenging, with lactylation potentially playing a key role. This study investigated lactylation-related genes (LRGs) in HIBD.
methodsHIBD models used SD rats. Transcriptomics, proteomics, and scRNA-seq analyzed brain tissues across time points. Machine learning integrated DEGs/DEPs and LRG data to identify a biomarker. Inflammation (IL-1β, ELISA), oxidative stress (MDA, CAT), histopathology (HE, Nissl staining), and long-term function (Morris water maze) were assessed. Molecular docking predicted drug interactions.
resultsGFAP and LCP1 were identified as key up-regulated LRGs in HIBD, linked to ubiquitin-mediated proteolysis. Ginkgolide B and tangeretin significantly reduced acute inflammation (IL-1β), oxidative damage (MDA, CAT), improved histopathology, and enhanced long-term cognitive outcomes. scRNA-seq revealed dynamic biomarker expression during astrocyte and microglial differentiation.
conclusionThe study defines GFAP and LCP1 as critical lactylation-associated therapeutic targets in HIBD. Ginkgolide B and tangeretin demonstrate potent neuroprotective effects, offering novel HIBD treatment strategies. IMPACT: We explored a rat pup model of neonatal hypoxic-ischemic encephalopathy using a multi-omics approach for the first time. We also investigated the role of lactate metabolism-related genes in this model, providing potential new targets and directions for future drug development.
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