Evidence map›Paper›PMID 28729364›Full record

ArticleArteriosclerosis, thrombosis, and vascular biology2017

TGF-β (Transforming Growth Factor-β) Signaling Protects the Thoracic and Abdominal Aorta From Angiotensin II-Induced Pathology by Distinct Mechanisms.

Stoyan N Angelov, Jie Hong Hu, Hao Wei, Nathan Airhart, Minghui Shi, David A Dichek

Open access · bronzeAbstract read
In one paragraph

Article in Arteriosclerosis, thrombosis, and vascular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.

0numbers the graph read from it
0cells of the map it votes in
80citing papers in PubMed
8.0field-weighted citation impact, top 2% 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

80 citing papers in PubMed, 117 citations in OpenAlex.

  1. Article
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  11. Transforming Growth Factors in Venous Thrombus Formation and Resolution.Arteriosclerosis, thrombosis, and vascular biology · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Article
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  17. Review
  18. Article
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20 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors at 1 institution in 1 country.

Stoyan N AngelovFrom the Department of Medicine, University of Washington School of Medicine, Seattle.
Jie Hong HuFrom the Department of Medicine, University of Washington School of Medicine, Seattle.
Hao WeiFrom the Department of Medicine, University of Washington School of Medicine, Seattle.
Nathan AirhartFrom the Department of Medicine, University of Washington School of Medicine, Seattle.
Minghui ShiFrom the Department of Medicine, University of Washington School of Medicine, Seattle.
David A DichekFrom the Department of Medicine, University of Washington School of Medicine, Seattle. ddichek@uw.edu.
University of Washington · US

Funding

Vector and Transgenic Mouse CoreP30DK017047 · NIDDK · UNIVERSITY OF WASHINGTON · PI Sakeneh Zraika · 1986 to 2026
$41.4M
CARDIOVASCULAR RESEARCH TRAINING PROGRAMT32HL007828 · NHLBI · UNIVERSITY OF WASHINGTON · PI Francis Kim, Farid Moussavi-Harami · 1997 to 2026
$10.2M
Roles of SMC TGF-beta Signaling in Aortic Health and Aneurysm FormationR01HL116612 · NHLBI · UNIVERSITY OF WASHINGTON · PI DICHEK, DAVID A · 2013 to 2016
$1.5M
NHLBI NIH HHS R01 HL116612NHLBI NIH HHS T32 HL007828NIDDK NIH HHS P30 DK017047
6 · The paper itself

Abstract

objectiveThe role of TGF-β (transforming growth factor-β) signaling in abdominal aortic aneurysm (AAA) formation is controversial. Others reported that systemic blockade of TGF-β by neutralizing antibodies accelerated AAA development in angiotensin II-infused mice. This result is consistent with other studies suggesting that TGF-β signaling prevents AAA. Development of a therapy for AAA that exploits the protective actions of TGF-β would be facilitated by identification of the mechanisms through which TGF-β prevents AAA. We hypothesized that TGF-β signaling prevents AAA by its actions on aortic medial smooth muscle cells. APPROACH AND

resultsWe compared the prevalence, severity, and histopathology of angiotensin II-induced AAA among control mice (no TGF-β blockade), mice with antibody-mediated systemic neutralization of TGF-β, and mice with genetically based smooth muscle-specific loss of TGF-β signaling. Surprisingly, we found that systemic-but not smooth muscle-specific-TGF-β blockade significantly increased the prevalence of AAA and tended to increase AAA severity, adventitial thickening, and aortic wall macrophage accumulation. In contrast, abdominal aortas of mice with smooth muscle-specific loss of TGF-β signaling differed from controls only in having a thinner media. We examined thoracic aortas of the same mice. Here we found that smooth muscle-specific loss of

conclusionOur results suggest that TGF-β signaling prevents both abdominal and thoracic aneurysmal disease but does so by distinct mechanisms. Smooth muscle extrinsic signaling protects the abdominal aorta and smooth muscle intrinsic signaling protects the thoracic aorta.

Indexed as

Angiotensin IISignal TransductionVascular RemodelingAdventitiaAnimalsAntibodiesAorta, AbdominalAorta, ThoracicAortic Aneurysm, AbdominalAortic Aneurysm, ThoracicDilatation, PathologicDisease Models, AnimalFemaleGenetic Predisposition to DiseaseMaleMice, Inbred C57BLAngiotensin IIAntibodiesProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IITgfb1 protein, mouseTgfb2 protein, mouseTgfb3 protein, mouseTransforming Growth Factor betaTransforming Growth Factor beta1Transforming Growth Factor beta2Transforming Growth Factor beta3aneurysmangiotensin IIaortamacrophagesmicesmooth muscleTGF-β

Identifiers

PMID28729364
PMCPMC5658248
OpenAlexW2736720321

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.