Evidence map›Paper›PMID 25878593›Full record

ArticleNeural regeneration research2015

Neuroprotective effects of SMADs in a rat model of cerebral ischemia/reperfusion.

Fang-Fang Liu, Chao-Ying Liu, Xiao-Ping Li, Sheng-Zhe Zheng, Qing-Quan Li, Qun Liu, Lei Song

Open access · goldAbstract read
In one paragraph

Article in Neural regeneration research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
0.5field-weighted citation impact, top 34% 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

20 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. International journal of molecular sciences · 2023
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  8. Review
  9. Small molecule C381 targets the lysosome to reduce inflammation and ameliorate disease in models of neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2022
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  17. Potential lung carcinogenicity induced by chronic exposure to PMEnvironmental science and pollution research international · 2017
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  19. Article
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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.

Fang-Fang LiuDepartment of Neurology, First Hospital of Jilin University, Changchun, Jilin Province, China.
Chao-Ying LiuDepartment of Respiratory Medicine, First Hospital of Jilin University, Changchun, Jilin Province, China.
Xiao-Ping LiDepartment of Pediatrics, First Hospital of Jilin University, Changchun, Jilin Province, China.
Sheng-Zhe ZhengDepartment of Neurology, Affiliated Hospital of Yanbian University, Yanbian, Jilin Province, China.
Qing-Quan LiDepartment of Hepatic-Biliary-Pancreatic Medicine, First Hospital of Jilin University, Changchun, Jilin Province, China.
Qun LiuDepartment of Neurology, First Hospital of Jilin University, Changchun, Jilin Province, China.
Lei SongDepartment of Respiratory Medicine, First Hospital of Jilin University, Changchun, Jilin Province, China.
Jilin University · CNFirst Hospital of Jilin University · CNYanbian University Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Previous studies have shown that up-regulation of transforming growth factor β1 results in neuroprotective effects. However, the role of the transforming growth factor β1 downstream molecule, SMAD2/3, following ischemia/reperfusion remains unclear. Here, we investigated the neuroprotective effects of SMAD2/3 by analyzing the relationships between SMAD2/3 expression and cell apoptosis and inflammation in the brain of a rat model of cerebral ischemia/reperfusion. Levels of SMAD2/3 mRNA were up-regulated in the ischemic penumbra 6 hours after cerebral ischemia/reperfusion, reached a peak after 72 hours and were then decreased at 7 days. Phosphorylated SMAD2/3 protein levels at the aforementioned time points were consistent with the mRNA levels. Over-expression of SMAD3 in the brains of the ischemia/reperfusion model rats via delivery of an adeno-associated virus containing the SMAD3 gene could reduce tumor necrosis factor-α and interleukin-1β mRNA levels, down-regulate expression of the pro-apoptotic gene, capase-3, and up-regulate expression of the anti-apoptotic protein, Bcl-2. The SMAD3 protein level was negatively correlated with cell apoptosis. These findings indicate that SMAD3 exhibits neuroprotective effects on the brain after ischemia/reperfusion through anti-inflammatory and anti-apoptotic pathways.

Indexed as

apoptosisbrain injurycerebral ischemiainflammationnerve regenerationneural regenerationneuroprotectionNSFC grantSMAD3transforming growth factor β1

Identifiers

PMID25878593
PMCPMC4396107
OpenAlexW2082609019

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.