HMOX1 interacts with BNIP3 to modulate neuronal ferroptosis after spinal cord ischemia-reperfusion injury via a mitophagy-dependent mechanism.

ABSTRACT: Spinal cord ischemia-reperfusion injury (SCIRI) is a severe secondary complication of trauma, spinal cord decompression, and thoracoabdominal aortic surgery. Ferroptosis, a regulated cell death pathway characterized by iron-dependent accumulation of lethal reactive oxygen species and lipid peroxidation, has been implicated in various pathological conditions. However, its precise role and molecular mechanisms in SCIRI remain unclear. In this study, we demonstrated that ferroptosis contributes to the pathophysiology of SCIRI. Heme oxygenase 1 (HMOX1) was upregulated in both SCIRI rats and neuronal cells subjected to hypoxia-reoxygenation. Genetic knockdown of HMOX1 in vivo and in vitro markedly attenuated neuronal ferroptosis, improving neurological function, whereas HMOX1 overexpression rep

SUBMITTER: Duan Y 

PROVIDER: S-EPMC12623955 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature