Evidence map›Paper›PMID 34789271›Full record

ArticleFluids and barriers of the CNS2021

The impact of chronic mild hypoxia on cerebrovascular remodelling; uncoupling of angiogenesis and vascular breakdown.

Sebok K Halder, Richard Milner

Open access · goldAbstract read
In one paragraph

Article in Fluids and barriers of the CNS, 2021. 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
1.0field-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

19 citing papers in PubMed, 19 citations in OpenAlex.

  1. Review
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  12. Astrogliosis in the GFAP-CreBiomolecules · 2024
    Article
  13. Fibrinogen and tumors.Frontiers in oncology · 2024
    Review
  14. 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
  15. Review
  16. Article
  17. Article
  18. Physiological and Pathological Remodeling of Cerebral Microvessels.International journal of molecular sciences · 2022
    Review
  19. 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.

Sebok K HalderSan Diego Biomedical Research Institute, 10865 Road to the Cure, Suite 100, San Diego, CA, 92121, USA.
Richard MilnerSan Diego Biomedical Research Institute, 10865 Road to the Cure, Suite 100, San Diego, CA, 92121, USA. rmilner@sdbri.org.ORCID http://orcid.org/0000-0002-3327-3609
San Diego Biomedical Research Institute · US

Funding

A vasculo-protective role for beta4 integrin in neuroinflammationR01NS103966 · NINDS · SCRIPPS RESEARCH INSTITUTE, THE · PI MILNER, D. RICHARD · 2018 to 2022
$2.1M
NINDS NIH HHS NS103966NINDS NIH HHS R01 NS103966
6 · The paper itself

Abstract

backgroundChronic mild hypoxia (CMH, 8% O

methodsTo answer this question, mice were exposed to CMH (8% O

resultsThe following was observed: (1) most endothelial proliferation and extravascular fibrinogen leak occurred in capillaries and to a lesser degree in venules, (2) much to our surprise, endothelial proliferation and extravascular fibrinogen leak never colocalized, (3) interestingly however, endothelial proliferation was strongly associated with an intravascular fibrinogen staining pattern not seen in stable blood vessels, (4) DiI perfusion studies revealed that angiogenic vessels were adequately perfused, suggesting that fibrinogen retention in angiogenic vessels is not due to temporary closure of the vessel, but more likely because fibrinogen is retained within the vessel wall, (5) bromodeoxyuridine (BrdU) labelling as a means to more permanently label proliferating endothelial cells, confirmed lack of any connection between endothelial proliferation and extravascular fibrinogen leak, while (6) in contrast, proliferating microglia were detected within extravascular leaks.

conclusionsTaken together, our findings support the concept that in the short-term, hypoxia-induced endothelial proliferation triggers transient fibrinogen deposition within the walls of angiogenic blood vessels, but no overt vascular leak occurs in these vessels. Importantly, endothelial proliferation and extravascular fibrinogen leaks never co-localize, demonstrating that extravascular leak is not an unwanted side-effect of angiogenic endothelial proliferation, but rather a dysfunctional vascular response to hypoxia that occurs in a distinct group of non-angiogenic blood vessels.

Indexed as

AnimalsBlood-Brain BarrierCerebrovascular DisordersDisease Models, AnimalEndothelium, VascularFemaleHypoxiaMaleMiceMice, Inbred C57BLNeovascularization, PathologicVascular RemodelingAngiogenesisBlood–brain barrier integrityBrainChronic mild hypoxiaFibrinogenVascular leak

Identifiers

PMID34789271
PMCPMC8597176
OpenAlexW3214288944

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.