Evidence map›Paper›PMID 32647973›Full record

ArticleMolecular neurobiology2020

Erythropoietin-Induced Autophagy Protects Against Spinal Cord Injury and Improves Neurological Function via the Extracellular-Regulated Protein Kinase Signaling Pathway.

Lin Zhong, Hui Zhang, Zheng-Fei Ding, Jian Li, Jin-Wei Lv, Zheng-Jun Pan, De-Xiang Xu, Zong-Sheng Yin

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed, 1 pooled it
3.2field-weighted citation impact, top 7% 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

12 citing papers in PubMed, 1 synthesis or guideline pooled it, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Lin ZhongDepartment of Orthopedics, The First Affiliated Hospital of Anhui Medical University, #218 Jixi Road, Hefei, 230022, China.
Hui ZhangDepartment of Orthopedics, The First Affiliated Hospital of Anhui Medical University, #218 Jixi Road, Hefei, 230022, China.
Zheng-Fei DingDepartment of Orthopedics, The First Affiliated Hospital of Anhui Medical University, #218 Jixi Road, Hefei, 230022, China.
Jian LiDepartment of Toxicology, School of Public Health, Anhui Medical University, #81 Mei Shan Road, Hefei, 230032, China.
Jin-Wei LvDepartment of Toxicology, School of Public Health, Anhui Medical University, #81 Mei Shan Road, Hefei, 230032, China.
Zheng-Jun PanDepartment of Orthopedics, The Third Affiliated Hospital of Anhui Medical University, Hefei, Anhui Province, China.
De-Xiang XuDepartment of Toxicology, School of Public Health, Anhui Medical University, #81 Mei Shan Road, Hefei, 230032, China. xudex@126.com.
Zong-Sheng YinDepartment of Orthopedics, The First Affiliated Hospital of Anhui Medical University, #218 Jixi Road, Hefei, 230022, China. yinzongshengahmu@sohu.com.ORCID https://orcid.org/0000-0002-1941-329X
Anhui Medical University · CN

Funding

National Natural Science Foundation of China 81672161National Natural Science Foundation of China 81871785
6 · The paper itself

Abstract

The objective of this study was to explore the neuroprotective molecular mechanisms of erythropoietin (EPO) in rats following spinal cord injury (SCI). First, a standard SCI model was established. After drug or saline treatment was administered, locomotor function was evaluated in rats using the Basso, Beattie, and Bresnahan (BBB) locomotor rating scale. H&E, Nissl, and TUNEL staining were performed to assess the ratio of cavities, number of motor neurons, and apoptotic cells in the damaged area. The relative protein and mRNA expressions were examined using western blot and qRT-PCR analyses, and the inflammatory markers, axon special protein, and neuromuscular junctions (NMJs) were detected by immunofluorescence. Both doses of EPO notably improved locomotor function, but high-dose EPO was more effective than low-dose EPO. Moreover, EPO reduced the cavity ratio, cell apoptosis, and motor neuron loss in the damaged area, but enhanced the autophagy level and extracellular-regulated protein kinase (ERK) activity. Treatment with an ERK inhibitor significantly prevented the effect of EPO on SCI, and an activator mimicked the benefits of EPO. Further investigation revealed that EPO promoted SCI-induced autophagy via the ERK signaling pathway. EPO activates autophagy to promote locomotor function recovery in rats with SCI via the ERK signaling pathway.

Indexed as

AutophagyMAP Kinase Signaling SystemAnimalsAnti-Inflammatory AgentsApoptosisCell SurvivalDown-RegulationErythropoietinInflammationMotor NeuronsNeuroprotective AgentsProtein Kinase InhibitorsRats, Sprague-DawleyRecovery of FunctionSpinal CordSpinal Cord InjuriesAnti-Inflammatory AgentsErythropoietinNeuroprotective AgentsProtein Kinase InhibitorsTOR Serine-Threonine KinasesAutophagyErythropoietin (EPO)Extracellular-regulated protein kinases (ERK)Spinal cord injury (SCI)

Identifiers

PMID32647973
OpenAlexW3042195526

What OpenQuestion holds

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Read underepoch 390

Registered trials

None linked

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.