Evidence map›Paper›PMID 36614118›Full record

ArticleInternational journal of molecular sciences2022

Therapeutic Effect of Rapamycin on TDP-43-Related Pathogenesis in Ischemic Stroke.

Yi-Syue Tsou, Jing-Huei Lai, Kai-Yun Chen, Cheng-Fu Chang, Chi-Chen Huang

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
2.0field-weighted citation impact, top 12% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

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  10. Endometriosis and the Hallmarks of Cancer.Reproductive sciences (Thousand Oaks, Calif.) · 2026
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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

5 authors at 3 institutions in 1 country.

Yi-Syue TsouPh.D. Program in Medical Neuroscience, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan.
Jing-Huei LaiCore Laboratory of Neuroscience, Office of R&D, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0003-2894-9325
Kai-Yun ChenPh.D. Program in Medical Neuroscience, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan.
Cheng-Fu ChangDepartment of Neurosurgery, Taipei City Hospital, Zhong Xiao Branch, Taipei 110, Taiwan.ORCID 0000-0002-3416-261X
Chi-Chen HuangPh.D. Program in Medical Neuroscience, College of Medical Science and Technology, Taipei Medical University, Taipei 110, Taiwan.ORCID 0000-0001-5410-8285
Taipei Medical University · TWTaipei City Hospital · TWTaipei Medical University Hospital · TW

Funding

Ministry of Science and Technology MOST 110-2320-B-038 -067 -MY3.Taipei Medical University Hospital 108TMU-SSH-13
6 · The paper itself

Abstract

Stroke is a major cause of death and disability across the world, and its detrimental impact should not be underestimated. Therapies are available and effective for ischemic stroke (e.g., thrombolytic recanalization and mechanical thrombectomy); however, there are limitations to therapeutic interventions. Recanalization therapy has developed dramatically, while the use of adjunct neuroprotective agents as complementary therapies remains deficient. Pathological TAR DNA-binding protein (TDP-43) has been identified as a major component of insoluble aggregates in numerous neurodegenerative pathologies, including ALS, FTLD and Alzheimer's disease. Here, we show that increased pathological TDP-43 fractions accompanied by impaired mitochondrial function and increased gliosis were observed in an ischemic stroke rat model, suggesting a pathological role of TDP-43 in ischemic stroke. In ischemic rats administered rapamycin, the insoluble TDP-43 fraction was significantly decreased in the ischemic cortex region, accompanied by a recovery of mitochondrial function, the attenuation of cellular apoptosis, a reduction in infarct areas and improvements in motor defects. Accordingly, our results suggest that rapamycin provides neuroprotective benefits not only by ameliorating pathological TDP-43 levels, but also by reversing mitochondrial function and attenuating cell apoptosis in ischemic stroke.

Indexed as

Amyotrophic Lateral SclerosisIschemic StrokeStrokeAnimalsApoptosisDNA-Binding ProteinsRatsSirolimusDNA-Binding ProteinsSirolimusischemic strokerapamycinTDP-43

Identifiers

PMID36614118
PMCPMC9820757
OpenAlexW4313471789

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.