LncRNA TCONS_00067339 as a key regulatory factor inducing decreased cell viability and ferroptosis in neonatal hypoxic-ischemic brain damage.

Abstract

Newborn hypoxic-ischemic brain damage (HIBD) is a major cause of mortality and neurological disabilities. Ferroptosis, characterized by lipid peroxidation, is implicated in HIBD pathogenesis. The role of lncRNA TCONS_00067339 in ferroptosis regulation in HIBD is understudied. This study investigates its mechanisms using a HIBD rat model and PC12 high differentiation cells oxygen-glucose deprivation (OGD) model. We identified upregulated lncRNA TCONS_00067339 in HIBD, associated with cells viability and ferroptosis-related mitochondrial changes. RNA sequencing revealed differential lncRNA expression in hippocampal, and enrichment analyses suggested involvement in ferroptosis pathways. Knockdown of lncRNA TCONS_00067339 increased OGD-treated PC12 cells viability and reduced cell death. These findings indicate that lncRNA TCONS_00067339 is a key regulator in ferroptosis and cell survival in HIBD, offering a potential target for therapeutic intervention.