Evidence map›Paper›PMID 28060852›Full record

ArticlePloS one2017

Contribution of Vascular Cells to Neointimal Formation.

Falei Yuan, Dong Wang, Kang Xu, Jixian Wang, Zhijun Zhang, Li Yang, Guo-Yuan Yang, Song Li

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. 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
2.8field-weighted citation impact, top 9% 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, 41 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Circulation · 2021
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  9. Calciprotein Particles: Balancing Mineral Homeostasis and Vascular Pathology.Arteriosclerosis, thrombosis, and vascular biology · 2021
    Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Moderate Alcohol Consumption Targets S100βAlcoholism, clinical and experimental research · 2020
    Article
  16. Review
  17. Review
  18. 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

8 authors at 4 institutions in 2 countries.

Falei YuanDepartment of Neurology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Dong WangDepartment of Bioengineering, University of California, Berkeley, California, United States of America.
Kang XuDepartment of Bioengineering, Chong Qing University, Chongqing, China.
Jixian WangDepartment of Neurology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Zhijun ZhangMed-X Research Institute and School of Biomedical Engineering, Shanghai Jiao Tong University, Shanghai, China.
Li YangDepartment of Bioengineering, Chong Qing University, Chongqing, China.
Guo-Yuan YangDepartment of Neurology, Ruijin Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China.
Song LiDepartment of Bioengineering, University of California, Berkeley, California, United States of America.
Shanghai Jiao Tong University · CNChongqing University · CNUniversity of California, Los Angeles · USRuijin Hospital · CN

Funding

Multipotent stem cells for tissue regenerationR01EB012240 · NIBIB · UNIVERSITY OF CALIFORNIA BERKELEY · PI LI, SONG · 2010 to 2013
$1.9M
In Situ Regeneration of Blood VesselR01HL121450 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LI, SONG · 2015 to 2018
$1.8M
Stem Cells in Vascular RemodelingR01HL117213 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI LI, SONG · 2013 to 2016
$1.4M
NHLBI NIH HHS R01 HL117213NHLBI NIH HHS R01 HL121450NIBIB NIH HHS R01 EB012240
6 · The paper itself

Abstract

The de-differentiation and proliferation of smooth muscle cells (SMCs) are widely accepted as the major contributor to vascular remodeling. However, recent studies indicate that vascular stem cells (VSCs) also play an important role, but their relative contribution remains to be elucidated. In this study, we used genetic lineage tracing approach to further investigate the contribution of SMCs and VSCs to neointimal thickening in response to endothelium denudation injury or artery ligation. In vitro and in vivo analysis of MYH11-cre/Rosa-loxP-RFP mouse artery showed that SMCs proliferated at a much slower rate than non-SMCs. Upon denudation or ligation injury, two distinct types of neointima were identified: Type-I neointimal cells mainly involved SMCs, while Type II mainly involved non-SMCs. Using Sox10-cre/Rosa-loxP-LacZ mice, we found that Sox10+ cells were one of the cell sources in neointima. In addition, lineage tracing using Tie2-cre/Rosa-LoxP-RFP showed that endothelial cells also contributed to the neointimal formation, but rarely transdifferentiated into mesenchymal lineages. These results provide a novel insight into the contribution of vascular cells to neointima formation, and have significant impact on the development of more effective therapies that target specific vascular cell types.

Indexed as

ActinsAnimalsBiomarkersCarotid ArteriesCarotid Artery InjuriesCell TransdifferentiationDisease Models, AnimalEndothelial CellsFemaleGene ExpressionGenes, ReporterMaleMiceMice, TransgenicMuscle, Smooth, VascularMyocytes, Smooth MuscleActa2 protein, mouseActinsBiomarkersSox10 protein, mouseSOXE Transcription Factors

Identifiers

PMID28060852
PMCPMC5218548
OpenAlexW2569385893

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.