Evidence map›Paper›PMID 32581764›Full record

ArticleFrontiers in aging neuroscience2020

Excessive Production of Transforming Growth Factor β1 Causes Mural Cell Depletion From Cerebral Small Vessels.

Taisuke Kato, Yumi Sekine, Hiroaki Nozaki, Masahiro Uemura, Shoichiro Ando, Sachiko Hirokawa, Osamu Onodera

Open access · goldAbstract read
In one paragraph

Article in Frontiers in aging neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.2field-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

15 citing papers in PubMed, 18 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Elevated TGFβ signaling contributes to cerebral small vessel disease in mouse models of Gould syndrome.Matrix biology : journal of the International Society for Matrix Biology · 2023
    Article
  11. Article
  12. Article
  13. Review
  14. Review
  15. 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

7 authors at 1 institution in 1 country.

Taisuke KatoDepartment of System Pathology for Neurological Disorders, Brain Science Branch, Brain Research Institute, Niigata University, Niigata, Japan.
Yumi SekineDepartment of Neurology, Clinical Neuroscience Branch, Brain Research Institute, Niigata University, Niigata, Japan.
Hiroaki NozakiDepartment of Neurology, Clinical Neuroscience Branch, Brain Research Institute, Niigata University, Niigata, Japan.
Masahiro UemuraDepartment of Neurology, Clinical Neuroscience Branch, Brain Research Institute, Niigata University, Niigata, Japan.
Shoichiro AndoDepartment of Neurology, Clinical Neuroscience Branch, Brain Research Institute, Niigata University, Niigata, Japan.
Sachiko HirokawaDepartment of Neurology, Clinical Neuroscience Branch, Brain Research Institute, Niigata University, Niigata, Japan.
Osamu OnoderaDepartment of Neurology, Clinical Neuroscience Branch, Brain Research Institute, Niigata University, Niigata, Japan.
Niigata University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

It is increasingly becoming apparent that cerebrovascular dysfunction contributes to the pathogenic processes involved in vascular dementia, Alzheimer's disease, and other neurodegenerative disorders. Under these pathologic conditions, the degeneration of cerebral blood vessels is frequently accompanied by a loss of mural cells from the vascular walls. Vascular mural cells play pivotal roles in cerebrovascular functions, such as regulation of cerebral blood flow and maintenance of the blood-brain barrier (BBB). Therefore, cerebrovascular mural cell impairment is involved in the pathophysiology of vascular-related encephalopathies, and protecting these cells is essential for maintaining brain health. However, our understanding of the molecular mechanism underlying mural cell abnormalities is incomplete. Several reports have indicated that dysregulated transforming growth factor β (TGFβ) signaling is involved in the development of cerebral arteriopathies. These studies have specifically suggested the involvement of TGFβ overproduction. Although cerebrovascular toxicity

Indexed as

cerebral small vesselmural cellspericytessmooth muscle cellsTGFβ

Identifiers

PMID32581764
PMCPMC7283554
OpenAlexW3034153070

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.