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作者

Cheng Su Xingzhi Jing Xiaoyang Liu Yuandong Shao Yong Zheng Xiaodong Liu Xingang Cui

作者单位

⁶Xinjiang Production and Construction Corps Fourth Division Hospital, Yining, Xinjiang, 835000, China ³P.S. Cheng Su, Xingzhi Jing and Xiaoyang Liu contributed equally to this study. ²Department of Spine Surgery, Zhoukou Orthopaedic Hospital, Zhoukou 466000, China ¹Department of Spine Surgery, Shandong Provincial Hospital affiliated to Shandong First Medical University, Jinan, Shandong 250000, China ⁴Department of Spine Surgery, Shandong Provincial Hospital, Shandong University, Jinan, Shandong 250000, China ⁵Department of Spine Surgery, Binzhou People’s Hospital. Binzhou, Shandong 256600, China

刊名

International Immunopharmacology

年份

2025

卷号

Vol.147

页码

113895

ISSN

1567-5769

关键词

Ferristatin II Ferroptosis HIF-1α Intervertebral disc degeneration Mitophagy Transferrin receptor 1.

摘要

Background Nucleus pulposus degeneration represents a significant contributing factor in the pathogenesis of intervertebral disc degeneration , and is a key underlying mechanism in several lumbar spine pathologies. Nevertheless, the precise mechanisms that govern NP degeneration remain unclear. A significant contributing factor to IVDD has been identified as ferroptosis. Nevertheless, its function in the degeneration of NP remains uncertain. The transferrin receptor inhibitor Ferristatin II h...更多

Background Nucleus pulposus degeneration represents a significant contributing factor in the pathogenesis of intervertebral disc degeneration , and is a key underlying mechanism in several lumbar spine pathologies. Nevertheless, the precise mechanisms that govern NP degeneration remain unclear. A significant contributing factor to IVDD has been identified as ferroptosis. Nevertheless, its function in the degeneration of NP remains uncertain. The transferrin receptor inhibitor Ferristatin II has been demonstrated to possess neuroprotective properties, which are conferred by its ability to suppress ferroptosis. It is therefore crucial to investigate the mechanisms by which Fer-II exerts its protective effects against NP degradation. Methods In order to investigate the protective effects of Fer-II, an IVDD rat model was developed by puncturing the rat tail in vivo. Human NP cells extracted with the aid of tert‐butyl hydroperoxide and ferric ammonium citrate interventions mimic the IVDD pathological environment in vitro. Results The present study demonstrates that Fer-II can delay nucleus pulposus degeneration and IVDD by inhibiting ferroptosis. This conclusion was reached through epidemiological studies and in vitro and in vivo experiments. Furthermore, Fer-II was observed to alleviate oxidative stress-induced NP cell degeneration by activating the HIF-1α pathway, enhancing mitophagy, suppressing NP cell ferroptosis. Conclusions The findings of our study indicate that Fer-II has the potential to safeguard nucleus pulposus cells from degeneration by triggering HIF-1α-mediated mitophagy. The potential of Fer-II as a promising alternative therapeutic option for the management of IVDD is worthy of further investigation.收起

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