Evidence map›Paper›PMID 29416039›Full record

ArticleCell death & disease2018

bFGF plays a neuroprotective role by suppressing excessive autophagy and apoptosis after transient global cerebral ischemia in rats.

Dawei Sun, Wenying Wang, Xintao Wang, Yan Wang, Xiaotao Xu, Feng Ping, Yu Du, Wei Jiang, Derong Cui

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
6.2field-weighted citation impact, top 3% 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

37 citing papers in PubMed, 88 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

9 authors at 1 institution in 1 country.

Dawei SunDepartment of Anesthesiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.ORCID 0000-0002-6631-8527
Wenying WangDepartment of Anesthesiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Xintao WangDepartment of Anesthesiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Yan WangDepartment of Anesthesiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Xiaotao XuDepartment of Anesthesiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Feng PingDepartment of Anesthesiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Yu DuDepartment of Neurology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, 200233, Shanghai, China.
Wei JiangDepartment of Anesthesiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, 200233, Shanghai, China. jiangw@sjtu.edu.cn.
Derong CuiDepartment of Anesthesiology, Shanghai Jiaotong University Affiliated Sixth People's Hospital, 200233, Shanghai, China. cuishuning118@163.com.
Shanghai Sixth People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transient global cerebral ischemia (tGCI) is a cerebrovascular disorder that can cause apoptotic neuronal damage and functional deficits. Basic fibroblast growth factor (bFGF) was reported to be highly expressed in the central nervous system (CNS) and to exert neuroprotective effects against different CNS diseases. However, the effects of bFGF on tGCI have not been studied intensively. This study was conducted to investigate the effect of bFGF and its underlying mechanism in an animal model of tGCI. After intracerebroventricular (i.c.v.) injection of bFGF, functional improvement was observed, and the number of viable neurons increased in the ischemia-vulnerable hippocampal CA1 region. Apoptosis was induced after tGCI and could be attenuated by bFGF treatment via inhibition of p53 mitochondrial translocation. In addition, autophagy was activated during this process, and bFGF could inhibit activation of autophagy through the mTOR pathway. Rapamycin, an activator of autophagy, was utilized to explore the relationship among bFGF, apoptosis, and autophagy. Apoptosis deteriorated after rapamycin treatment, which indicated that excessive autophagy could contribute to the apoptosis process. In conclusion, these results demonstrate that bFGF could exert neuroprotective effects in the hippocampal CA1 region by suppressing excessive autophagy via the mTOR pathway and inhibiting apoptosis by preventing p53 mitochondrial translocation. Furthermore, our results suggest that bFGF may be a promising therapeutic agent to for treating tGCI in response to major adverse events, including cardiac arrest, shock, extracorporeal circulation, traumatic hemorrhage, and asphyxiation.

Indexed as

AnimalsApoptosisAutophagyBehavior, AnimalConditioning, PsychologicalFearFibroblast Growth Factor 2HippocampusIschemic Attack, TransientMaleMemoryMitochondriaNeuroprotective AgentsProtein TransportRats, Sprague-DawleySignal TransductionFibroblast Growth Factor 2Neuroprotective AgentsTOR Serine-Threonine KinasesTumor Suppressor Protein p53

Identifiers

PMID29416039
PMCPMC5833346
OpenAlexW2792601526

What OpenQuestion holds

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LicenceCC BY
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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.