Evidence map›Paper›PMID 31620993›Full record

ArticleMolecular neurobiology2020

Attenuation of Ischemic Stroke-Caused Brain Injury by a Monoamine Oxidase Inhibitor Involves Improved Proteostasis and Reduced Neuroinflammation.

Yanying Liu, Shelley Feng, Kalpana Subedi, Hongmin Wang

Open access · greenAbstract read
In one paragraph

Article in Molecular neurobiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
3.7field-weighted citation impact, top 6% 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, 55 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Review
  6. Article
  7. Article
  8. Advances in the study of the glymphatic system and aging.CNS neuroscience & therapeutics · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Review
  14. Review
  15. Stroke-Heart Syndrome: Recent Advances and Challenges.Journal of the American Heart Association · 2022
    Review
  16. Impact of Cardiovascular Diseases on Ischemic Stroke Outcomes.Journal of integrative neuroscience · 2022
    Review
  17. GABAInternational journal of molecular sciences · 2022
    Article
  18. Article
  19. Review
  20. Article
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

4 authors at 1 institution in 1 country.

Yanying LiuDivision of Basic Biomedical Sciences and Center for Brain and Behavior Research, Sanford School of Medicine, University of South Dakota, Vermillion, SD, 57069, USA.
Shelley FengDivision of Basic Biomedical Sciences and Center for Brain and Behavior Research, Sanford School of Medicine, University of South Dakota, Vermillion, SD, 57069, USA.
Kalpana SubediDivision of Basic Biomedical Sciences and Center for Brain and Behavior Research, Sanford School of Medicine, University of South Dakota, Vermillion, SD, 57069, USA.
Hongmin WangDivision of Basic Biomedical Sciences and Center for Brain and Behavior Research, Sanford School of Medicine, University of South Dakota, Vermillion, SD, 57069, USA. Hongmin.Wang@usd.edu.ORCID http://orcid.org/0000-0002-0392-4458
University of South Dakota · US

Funding

Role of ubiquilin in ischemic strokeR01NS088084 · NINDS · UNIVERSITY OF SOUTH DAKOTA · PI WANG, HONGMIN · 2015 to 2019
$1.4M
NINDS NIH HHS NS088084NINDS NIH HHS R01 NS088084
6 · The paper itself

Abstract

Mitochondrial dysfunction and oxidative stress play a key role in ischemia/reperfusion (I/R) induced brain injury. We previously showed that ubiquilin-1 (Ubqln1), a ubiquitin-like protein, improves proteostasis and protects brains against oxidative stress and I/R induced brain injury. We demonstrate here that nialamide (NM), a non-selective monoamine oxidase (MAO) inhibitor, upregulated Ublqn1 and protected neurons from oxygen-glucose deprivation- and I/R-caused cell death in in vitro and in vivo, respectively. Post-ischemic administration of the NM in a stroke mouse model even at 3 h following I/R still reduced neuronal injury and improved functional recovery and survival. Treating stroke animals with NM also increased the association of Ubqln1 with mitochondria and decreased the total oxidized and polyubiquitinated protein levels. Intriguingly, NM-enhanced proteostasis was also associated with reduced I/R-caused neuroinflammation, as reflected by attenuated activation of microglia and astrocytes as well as reduced TNF-α level. Thus, our results suggest that MAO inhibition-induced neuroprotection following I/R involves improved proteostasis and reduced neuroinflammation.

Indexed as

AnimalsAstrocytesBrainBrain InjuriesInflammationMiceMitochondriaMonoamine Oxidase InhibitorsNeuronsOxidative StressProteostasisRecovery of FunctionStrokeMonoamine Oxidase InhibitorsMitochondriaMonoamine oxidase inhibitorNeuroinflammationOxidative stressProteostasisUbiquilin

Identifiers

PMID31620993
PMCPMC7035161
OpenAlexW2980741649

What OpenQuestion holds

Textmetadata
LicenceTDM
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.