Evidence map›Paper›PMID 25448157›Full record

ArticleExperimental neurology2015

Defining the critical hypoxic threshold that promotes vascular remodeling in the brain.

Amin Boroujerdi, Richard Milner

Open access · greenAbstract read
In one paragraph

Article in Experimental neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 25% 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

20 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
  2. Review
  3. Relationship between Hypoxia and Hypercapnia Tolerance and Life Expectancy.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Intermittent hypoxia protects against hypoxic-ischemic brain damage by inducing functional angiogenesis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
    Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Hypoxia induces de novo formation of cerebral collaterals and lessens the severity of ischemic stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2020
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Amin BoroujerdiDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.
Richard MilnerDepartment of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA. Electronic address: rmilner@scripps.edu.
Scripps Research Institute · US

Funding

An angiogenic role for the alpha 5 beta 1 and alpha V beta 3 integrins during cerR01NS060770 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI MILNER, D. RICHARD · 2008 to 2012
$1.9M
NINDS NIH HHS NS060770NINDS NIH HHS R01 NS060770
6 · The paper itself

Abstract

In animal models, hypoxic pre-conditioning confers protection against subsequent neurological insults, mediated in part through an extensive vascular remodeling response. In light of the therapeutic potential of this effect, the goal of this study was to establish the dose-response relationship between level of hypoxia and the extent of cerebrovascular modeling, and to define the mildest level of hypoxia that promotes remodeling. Mice were exposed to different levels of continuous hypoxia (8-21% O2) for seven days before several aspects of vascular remodeling were evaluated, including endothelial proliferation, total vascular area, arteriogenesis, and fibronectin/α5β1 integrin expression. For most events, the threshold level of hypoxia that stimulated remodeling was 12-13% O2. Interestingly, many parameters displayed a biphasic dose-response curve, with peak levels attained at 10% O2, but declined thereafter. Further analysis in the 12-13% O2 range revealed that vascular remodeling occurs by two separate mechanisms: (i) endothelial hyperplasia, triggered by a hypoxic threshold of 13% O2, which leads to increased capillary growth, and (ii) endothelial hypertrophy, triggered by a more severe hypoxic threshold of 12% O2, which leads to expansion of large vessels and arteriogenesis. Taken together, these results define the hypoxic thresholds for vascular remodeling in the brain, and point to two separate mechanisms mediating this process.

Indexed as

AnimalsBrainCell ProliferationEndothelial CellsHypoxia, BrainImmunohistochemistryIschemic PreconditioningMiceMice, Inbred C57BLNeovascularization, PhysiologicVascular RemodelingAngiogenesisArteriogenesisBlood–brain barrier (BBB)Dose–responseEndothelial cellsFibronectinHypoxic thresholdVascular remodelingα5 integrin

Identifiers

PMID25448157
PMCPMC4261640
OpenAlexW2014541174

What OpenQuestion holds

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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.