Evidence map›Paper›PMID 24460674›Full record

ReviewBritish journal of pharmacology2014

Midkine in repair of the injured nervous system.

Yoshihiro Yoshida, Harutoshi Sakakima, Fumiyo Matsuda, Masako Ikutomo

Open access · hybridAbstract readReview
In one paragraph

Review in British journal of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. GLP-1R agonist semaglutide protects human forebrain organoids from cholesterol-induced neurotoxicity.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
    Article
  2. Review
  3. Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. The role of midkine in health and disease.Frontiers in immunology · 2023
    Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Axonal and Myelin Neuroprotection by the Peptoid BN201 in Brain Inflammation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Article
  18. Review
  19. Review
  20. Wnt/β-catenin up-regulates Midkine expression in glioma cells.International journal of clinical and experimental medicine · 2015
    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 2 institutions in 2 countries.

Yoshihiro YoshidaSchool of Health Sciences, Faculty of Medicine, Kagoshima University, Kagoshima, Japan.
Harutoshi Sakakima
Fumiyo Matsuda
Masako Ikutomo
RMIT University · AUKagoshima University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

unlabelledMidkine (MK) is a growth factor with neurotrophic and neurite outgrowth activities. It was expressed in the peri-ischaemic area in the acute phase of cerebral infarction in rat brains. Astrocytes were the origin of MK in this occasion. MK has been assessed in terms of its effects on neural injury. The administration of MK into the lateral ventricle immediately prior to ischaemia prevented cell death in the hippocampal CA1 neurons degenerated by transient forebrain ischaemia in gerbils. MK administration was also beneficial in rats with neural injury, especially after kainic acid-induced seizures. Gene therapy with mouse MK cDNA using an adenovirus was effective in reducing the cerebral infarction volume and in increasing the number of neuronal precursor cells in the subventricular zone of the rat brain. MK mRNA and MK protein were found in spinal cord motor neurons of the anterior horn in both the acute phase of sciatic nerve injury and 3 weeks later. MK immunoreactivity was also found in the proximal side of a sciatic nerve-injured site in sciatic nerve axons. MK receptors were expressed in Schwann cells after injury, suggesting crosstalk between axons and Schwann cells. MK was also present in nerve terminals and influenced ACh receptor clustering during neuromuscular development in Xenopus. Thus, MK may also be involved in reinforcing and maintaining the synapse. All these findings indicate the therapeutic potential of MK for promoting repair of the nervous system after injury. LINKED ARTICLES: This article is part of a themed section on Midkine. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-4.

Indexed as

AnimalsBrain InjuriesCytokinesHumansMidkineNerve Growth FactorsSciatic NerveCytokinesMidkineNerve Growth Factorscerebral infarctionmidkinemuscular injurynerve injuryneurotrophic factorsciatic nerve

Identifiers

PMID24460674
PMCPMC3925031
OpenAlexW1606217335

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.