Neurochem Res. 2026 Jan 20;51(1):53. doi: 10.1007/s11064-026-04667-0.
ABSTRACT
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.
PMID:41557190 | DOI:10.1007/s11064-026-04667-0