Evidence map›Paper›PMID 34967104›Full record

ArticleCNS neuroscience & therapeutics2022

Effect of axitinib regulating the pathological blood-brain barrier functional recovery for glioblastoma therapeutics.

Fengtian Zhang, Lijuan Wen, Kai Wang, Zhihua Huang, Xiangyu Jin, Ruiwen Xiong, Shiying He, Fuqiang Hu

Open access · goldAbstract read
In one paragraph

Article in CNS neuroscience & therapeutics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.3field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 16 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Article
  9. CD31 as a probable responding and gate-keeping protein of the blood-brain barrier and the risk of Alzheimer's disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Review
  10. 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 3 institutions in 1 country.

Fengtian ZhangMedical College of Soochow University, 199 Renai Road, Suzhou Industrial Park, Suzhou, China.
Lijuan WenCollege of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.ORCID 0000-0001-8070-0338
Kai WangCollege of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Zhihua HuangDepartment of Physiology, School of Basic Medical Sciences, Institute for Medical Sciences of Pain, Gannan Medical University, Ganzhou, China.
Xiangyu JinCollege of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Ruiwen XiongNational Engineering Research Center for Modernization of Tranditional Chinese Medicine-Hakka Medical Resources Branch, College of Pharmacy, Gannan Medical University, Ganzhou, China.
Shiying HeNational Engineering Research Center for Modernization of Tranditional Chinese Medicine-Hakka Medical Resources Branch, College of Pharmacy, Gannan Medical University, Ganzhou, China.
Fuqiang HuCollege of Pharmaceutical Sciences, Zhejiang University, Hangzhou, China.
Gannan Medical University · CNZhejiang University · CNSoochow University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsDysfunction of the blood-brain barrier (BBB) is a prominent pathological feature of glioblastoma (GBM). Vascular endothelial growth factor (VEGF) is confirmed to be abnormally elevated in the pathogenesis of GBM, causing BBB pathological disruption, which further allows the leakage of neurotoxic blood-derived molecules into the central nervous system (CNS), interfering brain homeostasis and leading to poor patient outcome. Since BBB is an integral and pivotal part of the brain microenvironment, which strongly supports the occurrence and the pathological progression of GBM, here we have selected the VEGFR antagonist axitinib as a BBB functional regulator and hypothesized to regulate pathological BBB restoration for GBM effective treatment.

methodsThe pathological BBB cell model was constructed to investigate the timeliness and dose effect of axitinib regulating pathological BBB restoration. In order to investigate the efficacy and safety of axitinib regulating pathological BBB restoration for anti-GBM treatment, the orthotropic GBM-bearing mice model was established for in vivo study, and bioluminescent imaging was used to real-time and noninvasively monitor tumor growth response in vivo, and survival time was also recorded.

resultsAxitinib under non-cytotoxic dosage regulated pathological BBB restoration in a time-dependent mode, and multiple intervention of axitinib could realize a visible restoration of pathological BBB in vitro. Moreover, axitinib treatment restored pathological BBB in orthotropic GBM-bearing mice. We further confirmed that functional restoration of pathological BBB with axitinib had certain curative effect in prolonging median survival of orthotropic GBM-bearing mice at non-cytotoxic dosages in vivo.

conclusionThe mechanism of axitinib involved in BBB functional regulation in the treatment of GBM is first illuminated in this report; moreover, this is the first report first referring to regulating pathological BBB functional recovery for GBM effective therapeutics. Overall, the view of regulating pathological BBB functional recovery may offer a novel sight for other CNS diseases relating to BBB permeability effective therapeutics.

Indexed as

Brain NeoplasmsGlioblastomaAnimalsAxitinibBlood-Brain BarrierCell Line, TumorMiceTumor MicroenvironmentVascular Endothelial Growth Factor AAxitinibVascular Endothelial Growth Factor Ablood-brain barrierglioblastomapathological disruptionrestorationtherapeutics

Identifiers

PMID34967104
PMCPMC8841308
OpenAlexW4200071400

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.