Evidence map›Paper›PMID 27923978›Full record

ArticlePhysiological reports2016

Smooth muscle cell-specific Tgfbr1 deficiency attenuates neointimal hyperplasia but promotes an undesired vascular phenotype for injured arteries.

Mingmei Liao, Pu Yang, Fen Wang, Scott A Berceli, Yasmin H Ali, Kelvin L Chan, Zhihua Jiang

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.3field-weighted citation impact, top 30% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Promoters to Study Vascular Smooth Muscle.Arteriosclerosis, thrombosis, and vascular biology · 2019
    Review
  5. 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 3 institutions in 2 countries.

Mingmei LiaoDivision of Vascular Surgery and Endovascular Therapy, University of Florida College of Medicine, Gainesville, Florida.
Pu YangDepartment of Surgery, Central South University Xiangya Hospital, Changsha, Hunan, China.
Fen WangDivision of Vascular Surgery and Endovascular Therapy, University of Florida College of Medicine, Gainesville, Florida.
Scott A BerceliDivision of Vascular Surgery and Endovascular Therapy, University of Florida College of Medicine, Gainesville, Florida.
Yasmin H AliDivision of Vascular Surgery and Endovascular Therapy, University of Florida College of Medicine, Gainesville, Florida.
Kelvin L ChanDivision of Vascular Surgery and Endovascular Therapy, University of Florida College of Medicine, Gainesville, Florida.
Zhihua JiangDivision of Vascular Surgery and Endovascular Therapy, University of Florida College of Medicine, Gainesville, Florida jiangzh@surgery.ufl.edu.
University of Florida · USFlorida College · USXiangya Hospital Central South University · CN

Funding

The Dichotomy of Alk1 and Alk5 Signaling Pathways in Vascular Response to InjuryR01HL105764 · NHLBI · UNIVERSITY OF FLORIDA · PI JIANG, ZHIHUA · 2011 to 2015
$1.6M
NHLBI NIH HHS R01 HL105764
6 · The paper itself

Abstract

Neointimal hyperplasia (NIH) and inward wall remodeling cause arterial restenosis and failure of bypass vein grafts. Previous studies from our group suggest that transforming growth factor (TGF) β promotes these pathologies via regulating cell kinetics at the early stage and matrix metabolism at the late stage. Although these temporal TGFβ effects may result from its signaling in different cell groups, the responsible cell type has not been identified. In the current study, we evaluated the effect of smooth muscle cell (SMC)-specific TGFβ signaling through its type I receptor TGFBR1 on NIH and wall remodeling of the injured femoral arteries (FAs). An inducible Cre/loxP system was employed to delete SMC Tgfbr1 (Tgfbr1

Indexed as

PhenotypeAnimalsApoptosisCell ProliferationCollagenFemoral ArteryGene DeletionHyperplasiaMaleMatrix Metalloproteinase 9MiceMice, Inbred C57BLMyocytes, Smooth MuscleNeointimaProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaCollagenMatrix Metalloproteinase 9Mmp9 protein, mouseProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type ITgfbr1 protein, mouseArterial restenosisinducible gene deletionreceptortransforming growth factor βvascular phenotype

Identifiers

PMID27923978
PMCPMC5357823
OpenAlexW2560370517

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.