Evidence map›Paper›PMID 29295709›Full record

ArticleJournal of biomedical science2018

Differential regulations of fibronectin and laminin in Smad2 activation in vascular endothelial cells in response to disturbed flow.

Tung-Lin Yang, Pei-Ling Lee, Ding-Yu Lee, Wei-Li Wang, Shu-Yi Wei, Chih-I Lee, Jeng-Jiann Chiu

Open access · diamondAbstract read
In one paragraph

Article in Journal of biomedical science, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
4.5field-weighted citation impact, top 5% 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, 1 synthesis or guideline pooled it, 60 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Vascular Extracellular Matrix in Atherosclerosis.International journal of molecular sciences · 2024
    Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Vascular mechanotransduction.Physiological reviews · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. Review
  15. Activation of Smad2/3 signaling by low fluid shear stress mediates artery inward remodeling.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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

7 authors at 1 institution in 1 country.

Tung-Lin YangDepartment of Life Sciences, National Central University, Jung-Li, Taoyuan, Taiwan.
Pei-Ling LeeInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli, Taiwan.
Ding-Yu LeeInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli, Taiwan.
Wei-Li WangInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli, Taiwan.
Shu-Yi WeiInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli, Taiwan.
Chih-I LeeInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli, Taiwan.
Jeng-Jiann ChiuInstitute of Cellular and System Medicine, National Health Research Institutes, Miaoli, Taiwan. jjchiu@nhri.org.tw.
National Health Research Institutes · TW

Funding

Ministry of Science and Technology in Taiwan MOST-105-2321-B-400-007Ministry of Science and Technology in Taiwan MOST-106-2633-B-009-001Ministry of Science and Technology in Taiwan MOST-106-3114-Y-043-021
6 · The paper itself

Abstract

backgroundAtherosclerosis occurs in arterial curvatures and branches, where the flow is disturbed with low and oscillatory shear stress (OSS). The remodeling and alterations of extracellular matrices (ECMs) and their composition is the critical step in atherogenesis. In this study, we investigated the effects of different ECM proteins on the regulation of mechanotransduction in vascular endothelial cells (ECs) in response to OSS.

methodsThrough the experiments ranging from in vitro cell culture studies on effects of OSS on molecular signaling to in vivo examinations on clinical specimens from patients with coronary artery disease (CAD), we elucidated the roles of integrins and different ECMs, i.e., fibronectin (FN) and laminin (LM), in transforming growth factor (TGF)-β receptor (TβR)-mediated Smad2 activation and nuclear factor-κB (NF-κB) signaling in ECs in response to OSS and hence atherogenesis.

resultsOSS at 0.5±12 dynes/cm

conclusionsOur findings provide new insights into the mechanisms of how OSS regulates Smad2 signaling and pro-inflammatory genes through the complex signaling networks of integrins, TβRs, and ECMs, thus illustrating the molecular basis of regional pro-inflammatory activation within disturbed flow regions in the arterial tree.

Indexed as

Mechanotransduction, CellularBiomechanical PhenomenaCells, CulturedEndothelial CellsExtracellular Matrix ProteinsFibronectinsHumansLamininSmad2 ProteinStress, MechanicalExtracellular Matrix ProteinsFibronectinsLamininSmad2 ProteinSMAD2 protein, humanEndothelial cellExtracellular matrixIntegrinShear stressTransforming growth factor receptor

Identifiers

PMID29295709
PMCPMC5749020
OpenAlexW2782144965

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.