Evidence map›Paper›PMID 24323729›Full record

ReviewTranslational stroke research2014

Phenotypic transformation of smooth muscle in vasospasm after aneurysmal subarachnoid hemorrhage.

Norihito Shimamura, Hiroki Ohkuma

Abstract readReview
PubMed Publisher
In one paragraph

Review in Translational stroke research, 2014. 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
3.5field-weighted citation impact, top 8% 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, 49 citations in OpenAlex.

  1. Haemorrhage, hypercoagulability and ischaemia: Evolution of brain injury after aneurysmal subarachnoid haemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2026
    Review
  2. Pathophysiology, Management, and Therapeutics in Subarachnoid Hemorrhage and Delayed Cerebral Ischemia: An Overview.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Review
  10. PDGFR-β modulates vascular smooth muscle cell phenotype via IRF-9/SIRT-1/NF-κB pathway in subarachnoid hemorrhage rats.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2019
    Article
  11. Article
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  15. The rise of soluble platelet-derived growth factor receptor β in CSF early after subarachnoid hemorrhage correlates with cerebral vasospasm.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2018
    Article
  16. Article
  17. Article
  18. Recanalization, reperfusion, and recirculation in stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
  19. Article
  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

2 authors at 1 institution in 1 country.

Norihito ShimamuraDepartment of Neurosurgery, Hirosaki University School of Medicine, 5-Zaihuchou, Hirosaki, Aomori Prefecture, 036-8562, Japan, shimab@cc.hirosaki-u.ac.jp.
Hiroki Ohkuma
Hirosaki University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Differentiated smooth muscle cells (SMC) control vasoconstriction and vasodilation, but they can undergo transformation, proliferate, secret cytokines, and migrate into the subendotherial layer with adverse consequences. In this review, we discuss the phenotypic transformation of SMC in cerebral vasospasm after subarachnoid hemorrhage. Phenotypic transformation starts with an insult as caused by aneurysm rupture: Elevation of intracranial and blood pressure, secretion of norepinephrine, and mechanical force on an artery are factors that can cause aneurysm. The phenotypic transformation of SMC is accelerated by inflammation, thrombin, and growth factors. A wide variety of cytokines (e.g., interleukin (IL)-1β, IL-33, matrix metalloproteinases, nitric oxidase synthases, endothelins, thromboxane A2, mitogen-activated protein kinase, platelet-derived vascular growth factors, and vascular endothelial factor) all play roles in cerebral vasospasm (CVS). We summarize the correlations between various factors and the phenotypic transformation of SMC. A new target of this study is the transient receptor potential channel in CVS. Statin together with fasdil prevents phenotypic transformation of SMC in an animal model. Clazosentan prevents CVS and improves outcome in aneurysmal subarachnoid hemorrhage in a dose-dependent manner. Clinical trials of cilostazol for the prevention of phenotypic transformation of SMC have been reported, along with requisite experimental evidence. To conquer CVS in its complexity, we will ultimately need to elucidate its general, underlying mechanism.

Indexed as

AnimalsCilostazolHumansInflammationMuscle, Smooth, VascularMyocytes, Smooth MusclePhenotypeSubarachnoid HemorrhageTetrazolesVascular RemodelingVasodilator AgentsVasospasm, IntracranialCilostazolTetrazolesVasodilator Agents

Identifiers

PMID24323729
OpenAlexW1967251278

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.