Evidence map›Paper›PMID 33098065›Full record

ArticleNeurochemical research2020

CTRP3 Activates the AMPK/SIRT1-PGC-1α Pathway to Protect Mitochondrial Biogenesis and Functions in Cerebral Ischemic Stroke.

Jianfei Gao, Tingting Qian, Wei Wang

Abstract read
PubMed Publisher
In one paragraph

Article in Neurochemical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

30 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Review
  6. HYQTD Drug-containing Serum Alleviates HCurrent pharmaceutical biotechnology · 2026
    Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Review
  13. The critical role of Sirt1 in ischemic stroke.Frontiers in pharmacology · 2025
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Role of NADCellular and molecular neurobiology · 2023
    Review
  20. The Role of Adipokines in the Pathogenesis of Psoriasis.International journal of molecular sciences · 2023
    Review
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

3 authors at 3 institutions in 1 country.

Jianfei GaoDepartment of ICU, Linyi People's Hospital, Wohushan Road, Lanshan District, Linyi, 276002, Shandong, China.
Tingting QianSpecialty of Gerontology (Cardiovascular Diseases), Weifang Medical University, No. 7166, Baotongxi Street, Weicheng District, Weifang, 261000, Shandong, China.
Wei WangDepartment of Chinese Medicine Integrated Traditional Chinese Medicine and Western Medicine, 960 Hospital of PLA Joint Service Support Force, No. 25, Shifan Road, Tianqiao District, Jinan, 250031, Shandong, China. nanmen621020@163.com.ORCID http://orcid.org/0000-0001-9443-8780
Jining Traditional Chinese Medicine Hospital · CNLinyi People's Hospital · CNWeifang Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C1q/tumor necrosis factor-related protein-3 (CTRP3) had shown its angiogenesis and enhancement of mitochondrial biogenesis properties in the treatment of myocardial infarction, but its potential roles in cerebral ischemic stroke had not been fully understood. This study aimed to clarify the underlying mechanism of how CTRP3 regulated mitochondrial functions in hippocampal neuronal cells (HPPNCs) after oxygen-glucose deprivation (OGD)/reoxygenation (R) treatment. Results showed that impeded CTRP3 expression and weakened viability were detected in OGD/R treated HPPNCs. CTRP3 showed its ability to enhance the viability and inhibited apoptosis of HPPNCs after OGD/R treatment and it could also promote the mitochondrial biogenesis and physiological functions. Silencing of PGC-1α partially abolished the protective function of CTRP3 on mitochondria and CTRP3 mediated the expression of PGC-1α via the AMPK/SIRT1-PGC-1α pathway. These findings provided information that CTRP3 prevented mitochondria from OGD/R injury through activating the AMPK/SIRT1-PGC-1α pathway. Our study suggested that CTRP3 might have the potential to become an emerging protective agent applied in the reperfusion treatment of ischemic stroke.

Indexed as

AMP-Activated Protein KinasesApoptosisCell HypoxiaCell ProliferationHumansIschemic StrokeMitochondriaOrganelle BiogenesisPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaSignal TransductionSirtuin 1Tumor Necrosis FactorsAMP-Activated Protein KinasesC1QTNF3 protein, humanPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaPPARGC1A protein, humanSIRT1 protein, humanSirtuin 1Tumor Necrosis FactorsAMPK/SIRT1-PGC-1αCerebral ischemic strokeCTRP3MitochondriaOGD/R

Identifiers

PMID33098065
OpenAlexW3094275096

What OpenQuestion holds

Textmetadata
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.