Evidence map›Paper›PMID 27807406›Full record

ArticleFrontiers in cellular neuroscience2016

C1q/Tumor Necrosis Factor-Related Protein-3 Attenuates Brain Injury after Intracerebral Hemorrhage via AMPK-Dependent Pathway in Rat.

Shaohua Wang, Yang Zhou, Bo Yang, Lingyu Li, Shanshan Yu, Yanlin Chen, Jin Zhu, Yong Zhao

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
2.2field-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

19 citing papers in PubMed, 35 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Review
  12. Article
  13. Review
  14. Article
  15. The Eeffect of Metformin Combined with Calcium-Vitamin DAdvanced pharmaceutical bulletin · 2018
    Article
  16. Review
  17. Review
  18. Article
  19. 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

8 authors at 1 institution in 1 country.

Shaohua WangDepartment of Pathology, Chongqing Medical UniversityChongqing, China; Key Laboratory of Neurobiology, Chongqing Medical UniversityChongqing, China.
Yang ZhouDepartment of Pathology, Chongqing Medical UniversityChongqing, China; Key Laboratory of Neurobiology, Chongqing Medical UniversityChongqing, China.
Bo YangDepartment of Pathology, Chongqing Medical UniversityChongqing, China; Key Laboratory of Neurobiology, Chongqing Medical UniversityChongqing, China.
Lingyu LiDepartment of Pathology, Chongqing Medical UniversityChongqing, China; Key Laboratory of Neurobiology, Chongqing Medical UniversityChongqing, China.
Shanshan YuDepartment of Pathology, Chongqing Medical UniversityChongqing, China; Key Laboratory of Neurobiology, Chongqing Medical UniversityChongqing, China.
Yanlin ChenDepartment of Pathology, Chongqing Medical UniversityChongqing, China; Key Laboratory of Neurobiology, Chongqing Medical UniversityChongqing, China.
Jin ZhuDepartment of Pathology, Chongqing Medical UniversityChongqing, China; Key Laboratory of Neurobiology, Chongqing Medical UniversityChongqing, China.
Yong ZhaoDepartment of Pathology, Chongqing Medical UniversityChongqing, China; Key Laboratory of Neurobiology, Chongqing Medical UniversityChongqing, China.
Chongqing Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

C1q/tumor necrosis factor (TNF)-related protein-3 (CTRP3) is a recently discovered adiponectin paralog with established metabolic regulatory properties. However, the role of CTRP3 in intracerebral hemorrhage (ICH) is still mostly unresolved. The aim of the present report was to explore the possible neuroprotective effect of CTRP3 in an ICH rat model and to elucidate the fundamental mechanisms. ICH was induced in rats by intracerebral infusion of autologous arterial blood. The effects of exogenous CTRP3 (recombinant or lentivirus CTRP3) on brain injury were explored on day 7. Treatment with CTRP3 reduced brain edema, protected against disruption of the blood-brain barrier (BBB), improved neurological functions and promoted angiogenesis. Furthermore, CTRP3 greatly intensified phosphorylation of AMP-activated protein kinase (AMPK) in addition to expression of hypoxia inducing factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF). Finally, the protective effects of CTRP3 could be blocked by either AMPK or VEGF inhibitors. Our findings give the first evidence that CTRP3 is a new proangiogenic and neuroprotective adipokine, which may exert its protective effects at least partly through an AMPK/HIF-1α/ VEGF-dependent pathway, and suggest that CTRP3 may provide a new therapeutic strategy for ICH.

Indexed as

angiogenesisblood-brain barrier disruptionbrain edemaCTRP3intracerebral hemorrhageneuroprotection

Identifiers

PMID27807406
PMCPMC5069420
OpenAlexW2537482545

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.