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<p>Perinatal hypoxic–ischemic injury (HI) upregulated an endogenous retrovirus–derived lncRNA, EVADR, via HIF-1α/NF-κB. EVADR bound and repressed miR-145, thereby activating WNT/β-catenin signaling. Binding specificity was confirmed by biotin–miRNA pull-down and mutant-seed luciferase reporters. Genetic (si-CTNNB1/si-WNT3A) and pharmacologic (XAV939/CHIR99021) cross-validation demonstrated pathway necessity and rescue. EVADR gain-of-function reduced neuronal death and inflammation and improved behavioral outcomes following HI. Circulating EVADR levels in plasma/CSF correlated with injury severity; ROC analyses indicated diagnostic potential alone and combined with S100B/NSE. These data support EVADR–miR-145→WNT/β-catenin as a mechanistic axis with translational relevance.</p> Graphical Abstract <p></p>

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EVADR lncRNA Mitigates Neonatal Hypoxic–Ischemic Brain Injury via the miR-145→WNT/β-Catenin Axis and Exhibits Biomarker Potential

  • 期刊论文

  • 发表日期：

    2026年1月20日

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  • Sen Lu,
  • Mingbin Bao,
  • Junting Hu

摘要

Perinatal hypoxic–ischemic injury (HI) upregulated an endogenous retrovirus–derived lncRNA, EVADR, via HIF-1α/NF-κB. EVADR bound and repressed miR-145, thereby activating WNT/β-catenin signaling. Binding specificity was confirmed by biotin–miRNA pull-down and mutant-seed luciferase reporters. Genetic (si-CTNNB1/si-WNT3A) and pharmacologic (XAV939/CHIR99021) cross-validation demonstrated pathway necessity and rescue. EVADR gain-of-function reduced neuronal death and inflammation and improved behavioral outcomes following HI. Circulating EVADR levels in plasma/CSF correlated with injury severity; ROC analyses indicated diagnostic potential alone and combined with S100B/NSE. These data support EVADR–miR-145→WNT/β-catenin as a mechanistic axis with translational relevance.

Graphical Abstract