Evidence map›Paper›PMID 36171540›Full record

ArticleBMC neuroscience2022

Enhanced autophagy interacting proteins negatively correlated with the activation of apoptosis-related caspase family proteins after focal ischemic stroke of young rats.

Jie Wang, Zihao Xia, Peng Sheng, Mengmeng Shen, Lidong Ding, Dezhi Liu, Bing Chun Yan

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

Article in BMC neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.8field-weighted citation impact, top 28% 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

3 citing papers in PubMed, 5 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

7 authors at 3 institutions in 1 country.

Jie Wang *Medical College, Institute of Translational Medicine, Department of Neurology, Affiliated Hospital of Yangzhou University, Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, The Key Laboratory of Syndrome Differentiation and Treatment of Gastric Cancer of the State Administration of Traditional Chinese Medicine, Yangzhou University, Yangzhou, 225001, People's Republic of China.
Zihao Xia *Medical College, Institute of Translational Medicine, Department of Neurology, Affiliated Hospital of Yangzhou University, Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, The Key Laboratory of Syndrome Differentiation and Treatment of Gastric Cancer of the State Administration of Traditional Chinese Medicine, Yangzhou University, Yangzhou, 225001, People's Republic of China.
Peng ShengMedical College, Institute of Translational Medicine, Department of Neurology, Affiliated Hospital of Yangzhou University, Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, The Key Laboratory of Syndrome Differentiation and Treatment of Gastric Cancer of the State Administration of Traditional Chinese Medicine, Yangzhou University, Yangzhou, 225001, People's Republic of China.
Mengmeng ShenMedical College, Institute of Translational Medicine, Department of Neurology, Affiliated Hospital of Yangzhou University, Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, The Key Laboratory of Syndrome Differentiation and Treatment of Gastric Cancer of the State Administration of Traditional Chinese Medicine, Yangzhou University, Yangzhou, 225001, People's Republic of China.
Lidong DingDepartment of Neurology, Taizhou Second People's Hospital, Taizhou, 225500, People's Republic of China.
Dezhi LiuDepartment of Neurology, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, No.528 Zhang-Heng Road, Pu-Dong New Area, Shanghai, 201203, People's Republic of China. yzldz@126.com.
Bing Chun YanMedical College, Institute of Translational Medicine, Department of Neurology, Affiliated Hospital of Yangzhou University, Jiangsu Key Laboratory of Integrated Traditional Chinese and Western Medicine for Prevention and Treatment of Senile Diseases, The Key Laboratory of Syndrome Differentiation and Treatment of Gastric Cancer of the State Administration of Traditional Chinese Medicine, Yangzhou University, Yangzhou, 225001, People's Republic of China. bcyan@yzu.edu.cn.
Yangzhou University · CNShuguang Hospital · CNTaizhou Second People's Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeuronal injury induced in young rats by cerebral ischemia reperfusion (CIR) is known to differ substantially from that in adult rats. In the present study, we investigated the specific differences in neuronal injury induced by focal CIR between young and adult rats.

results2, 3, 5-triphenyl tetrazolium chloride (TTC) staining revealed a gradual increase in the infarct volume of both young and adult rats in accordance with I/R times and was significantly lower in young rats than in adult rats under the same conditions. The number of cells in the cortex showing immunoreactivity for neuronal nuclei (NeuN) gradually decreased in both young and adult rats in accordance with I/R times; these numbers were significantly higher in young rats than in adult rats under the same conditions. Similarly, as the duration of I/R increased, the degree of glial activation in the cortex penumbra region became more severe in both young and adult groups; however, glial activation was significantly lower in the cortex penumbra region of young rats when compared with that in adult rats. In addition, the expression of Beclin-1 was significantly higher in the infarct penumbra of young rats than adult rats and was more frequently co-expressed with neurons. The levels of autophagy-related proteins increased significantly in the penumbra region after I/R in both young and adult groups, this increase was more pronounced in young rats than in adult rats. Following CIR, analysis revealed significantly lower levels of pro-apoptosis-related factors and significantly higher levels of anti-apoptosis-related proteins in the young rats than in adult rats.

conclusionsCollectively, the present results suggest that the the reduced levels of neuronal death after CIR in young rats were closely related to enhanced levels of autophagy and reduced levels of pro-apoptosis in neurons.

Indexed as

Brain IschemiaIschemic StrokeReperfusion InjuryAnimalsApoptosis Regulatory ProteinsAutophagyBeclin-1Caspase 3CaspasesChloridesInfarctionRatsApoptosis Regulatory ProteinsBeclin-1Caspase 3CaspasesChloridesApoptosis-related proteinsAutophagy interacting proteinsNeuronal injuryYoung ischemic stroke

Identifiers

PMID36171540
PMCPMC9516802
OpenAlexW4297544421

What OpenQuestion holds

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LicenceCC BY
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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.