ER stress mediated‑autophagy contributes to neurological dysfunction in traumatic brain injury via the ATF6 UPR signaling pathway

A major public health problem, traumatic brain injury (TBI) can cause severe neurological impairment. Although autophagy is closely associated with the pathogenesis of TBI, role in deficits unclear. The purpose present study was to investigate molecular mechanisms endoplasmic reticulum (ER) stress‑induced and its detrimental effects on outcomes following TBI. rat model TBI established by controlled cortical impact. ER stress activation, induction autophagic flux dysfunction were examined damaged hippocampus post‑TBI. Pharmacological inhibition significantly blocked post‑traumatic as evidenced decreased conversion microtubule‑associated protein 1 light chain 3 (LC3)‑I LC3‑II Beclin‑1 expression levels region. Short hairpin RNA‑mediated activating transcription factor 6 knockdown prevented stress‑mediated stimulation via targeting essential genes, including related (ATG)3, ATG9 ATG12. Furthermore, scores, foot fault test Morris water maze used evaluate functions rats. results revealed that blockage or attenuated TBI‑induced damage functional outcomes. In conclusion, these findings provided new insights into demonstrated potential deficiency