Evidence map›Paper›PMID 29556174›Full record

ArticleFrontiers in neuroscience2018

Apolipoprotein E-Mimetic Peptide COG1410 Promotes Autophagy by Phosphorylating GSK-3β in Early Brain Injury Following Experimental Subarachnoid Hemorrhage.

Xinshen Li, Jianhua Peng, Jinwei Pang, Yue Wu, Xueping Huang, Yong Li, Jian Zhou, Long Gu, Xiaochuan Sun, Ligang Chen and 2 more

RetractedOpen access · goldAbstract readRetracted Publication
In one paragraph

Article in Frontiers in neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 10 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 14% 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

10 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.

  1. Pooled it
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  4. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 3 institutions in 2 countries.

Xinshen LiDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Jianhua PengDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Jinwei PangDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Yue WuDepartment of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Xueping HuangDepartment of Neurosurgery, Luzhou People's Hospital, Luzhou, China.
Yong LiDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Jian ZhouDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Long GuDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Xiaochuan SunDepartment of Neurosurgery, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Ligang ChenDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Michael P VitekMedicine, Duke University Medical Center, Durham, NC, United States.
Yong JiangDepartment of Neurosurgery, The Affiliated Hospital of Southwest Medical University, Luzhou, China.
Affiliated Hospital of Southwest Medical University · CNChongqing Medical University · CNDuke Medical Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

COG1410, a mimetic peptide derived from the apolipoprotein E (apoE) receptor binding region, exerts positive effect on neurological deficits in early brain injury (EBI) after experimental subarachnoid hemorrhage (SAH). Currently the neuroprotective effect of COG1410 includes inhibiting BBB disruption, reducing neuronal apoptosis, and neuroinflammation. However, the effect and mechanism of COG1410 to subcellular organelles disorder have not been fully investigated. As the main pathway for recycling long-lived proteins and damaged organelles, neuronal autophagy is activated in SAH and exhibits neuroprotective effects by reducing the insults of EBI. Pharmacologically elevated autophagy usually contributes to alleviated brain injury, while few of the agents achieved clinical transformation. In this study, we explored the activation of autophagy during EBI by measuring the Beclin-1 and LC3B-II protein levels. Administration of COG1410 notably elevated the autophagic markers expression in neurons, simultaneously reversed the neurological deficits. Furthermore, the up-regulated autophagy by COG1410 was further promoted by p-GSK-3β agonist, whereas decreased by p-GSK-3β inhibitor. Taken together, these data suggest that the COG1410 might be a promising therapeutic strategy for EBI via promoting autophagy in SAH.

Indexed as

apolipoprotein Eautophagyearly brain injuryglycogen synthase kinase 3 betasubarachnoid hemorrhage

Identifiers

PMID29556174
PMCPMC5844970
OpenAlexW2790725354

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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.