Evidence map›Paper›PMID 30539824›Full record

ArticleNeural regeneration research2019

Deferoxamine promotes recovery of traumatic spinal cord injury by inhibiting ferroptosis.

Xue Yao, Yan Zhang, Jian Hao, Hui-Quan Duan, Chen-Xi Zhao, Chao Sun, Bo Li, Bao-You Fan, Xu Wang, Wen-Xiang Li and 5 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 175 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
175citing papers in PubMed, 1 pooled it
5.0field-weighted citation impact, top 4% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

175 citing papers in PubMed, 1 synthesis or guideline pooled it, 289 citations in OpenAlex.

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  11. Crosstalk between autophagy and ferroptosis in liver diseases (Review).International journal of molecular medicine · 2026
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115 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 2 countries.

Xue YaoDepartment of Orthopedics, Tianjin Medical University General Hospital; State Key Laboratory of Medicinal Chemical Biology, Nankai University; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin, China.
Yan ZhangDepartment of Orthopedics, Tianjin Medical University General Hospital; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin, China.
Jian HaoDepartment of Orthopedics, Tianjin Medical University General Hospital; Department of Orthopedics, Nankai Hospital, Tianjin, China.
Hui-Quan DuanDepartment of Orthopedics, Tianjin Medical University General Hospital; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin, China.
Chen-Xi ZhaoDepartment of Orthopedics, Tianjin Medical University General Hospital; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin, China.
Chao SunDepartment of Orthopedics, Tianjin Medical University General Hospital; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin, China.
Bo LiDepartment of Orthopedics, Tianjin Medical University General Hospital; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin, China.
Bao-You FanDepartment of Orthopedics, Tianjin Medical University General Hospital; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin, China.
Xu WangDepartment of Orthopedics, Tianjin Medical University General Hospital; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin, China.
Wen-Xiang LiDepartment of Orthopedics, Tianjin Medical University General Hospital; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin, China.
Xuan-Hao FuDepartment of Orthopedics, Tianjin Medical University General Hospital; International Science and Technology Cooperation Base of Spinal Cord Injury, Tianjin, China.
Yong HuDepartment of Orthopedic and Traumatology, The University of Hong Kong, Pokfulam, Hong Kong Special Administrative Region, China.
Chang LiuSchool of Medicine, Nankai University, Tianjin, China.
Xiao-Hong KongSchool of Medicine, Nankai University, Tianjin, China.
Shi-Qing FengDepartment of Orthopedics, Tianjin Medical University General Hospital; International Science and Technology Cooperation Base of Spinal Cord Injury; Tianjin Neurological Institute, Key Laboratory of Post-Neuroinjury Neuro-repair and Regeneration in Central Nervous System, Ministry of Education and Tianjin City, Tianjin, China.
China International Science and Technology Cooperation · CNTianjin Medical University General Hospital · CNNankai University · CNTianjin Nankai Hospital · CNUniversity of Hong Kong · HK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ferroptosis is an iron-dependent novel cell death pathway. Deferoxamine, a ferroptosis inhibitor, has been reported to promote spinal cord injury repair. It has yet to be clarified whether ferroptosis inhibition represents the mechanism of action of Deferoxamine on spinal cord injury recovery. A rat model of Deferoxamine at thoracic 10 segment was established using a modified Allen's method. Ninety 8-week-old female Wistar rats were used. Rats in the Deferoxamine group were intraperitoneally injected with 100 mg/kg Deferoxamine 30 minutes before injury. Simultaneously, the Sham and Deferoxamine groups served as controls. Drug administration was conducted for 7 consecutive days. The results were as follows: (1) Electron microscopy revealed shrunken mitochondria in the spinal cord injury group. (2) The Basso, Beattie and Bresnahan locomotor rating score showed that recovery of the hindlimb was remarkably better in the Deferoxamine group than in the spinal cord injury group. (3) The iron concentration was lower in the Deferoxamine group than in the spinal cord injury group after injury. (4) Western blot assay revealed that, compared with the spinal cord injury group, GPX4, xCT, and glutathione expression was markedly increased in the Deferoxamine group. (5) Real-time polymerase chain reaction revealed that, compared with the Deferoxamine group, mRNA levels of ferroptosis-related genes Acyl-CoA synthetase family member 2 (ACSF2) and iron-responsive element-binding protein 2 (IREB2) were up-regulated in the Deferoxamine group. (6) Deferoxamine increased survival of neurons and inhibited gliosis. These findings confirm that Deferoxamine can repair spinal cord injury by inhibiting ferroptosis. Targeting ferroptosis is therefore a promising therapeutic approach for spinal cord injury.

Indexed as

astrogliosisdeferoxamineferroptosisGPX4ironlipid peroxidationnerve regenerationneural regenerationsecondary injuryspinal cord injurytreatmentxCT

Identifiers

PMID30539824
PMCPMC6334606
OpenAlexW2904457678

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.