Evidence map›Paper›PMID 28943527›Full record

ReviewJournal of atherosclerosis and thrombosis2018

Crossing Bridges between Extra- and Intra-Cellular Events in Thoracic Aortic Aneurysms.

Yoshito Yamashiro, Hiromi Yanagisawa

Open access · diamondAbstract readReview
In one paragraph

Review in Journal of atherosclerosis and thrombosis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.2field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Review
  3. Protective Role of Endothelial Fibulin-4 in Valvulo-Arterial Integrity.Journal of the American Heart Association · 2023
    Article
  4. Article
  5. Review
  6. Journal of the American Heart Association · 2021
    Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. The genetics and biomechanics of thoracic aortic diseases.Vascular biology (Bristol, England) · 2019
    Review
  15. Article
  16. Article
  17. 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

2 authors at 1 institution in 1 country.

Yoshito YamashiroLife Science Center of Tsukuba Advanced Research Alliance, University of Tsukuba.
Hiromi YanagisawaLife Science Center of Tsukuba Advanced Research Alliance, University of Tsukuba.
University of Tsukuba · JP

Funding

Loss of Matrix Regulation and Aortic Aneurysm Development in vivoR01HL106305 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI YANAGISAWA, HIROMI · 2011 to 2014
$1.5M
NHLBI NIH HHS R01 HL106305
6 · The paper itself

Abstract

Thoracic aortic aneurysms (TAAs) are common, life-threatening diseases and are a major cause of mortality and morbidity. Over the past decade, genetic approaches have revealed that 1) activation of the transforming growth factor beta (TGF-β) signaling, 2) alterations in the contractile apparatus of vascular smooth muscle cells (SMCs), and 3) defects in the extracellular matrix (ECM) were responsible for development of TAAs. Most recently, a fourth mechanism has been proposed in that dysfunction of mechanosensing in the aortic wall in response to hemodynamic stress may be a key driver of TAAs. Interestingly, the elastin-contractile unit, which is an anatomical and functional unit connecting extracellular elastic laminae to the intracellular SMC contractile filaments, via cell surface receptors, has been shown to play a critical role in the mechanosensing of SMCs, and many genes identified in TAAs encode for proteins along this continuum. However, it is still debated whether these four pathways converge into a common pathway. Currently, an effective therapeutic strategy based on the underlying mechanism of each type of TAAs has not been established. In this review, we will update the present knowledge on the molecular mechanism of TAAs with a focus on the signaling pathways potentially involved in the initiation of TAAs. Finally, we will evaluate current therapeutic strategies for TAAs and propose new directions for future treatment of TAAs.

Indexed as

AnimalsAortic Aneurysm, ThoracicExtracellular MatrixHumansMuscle, Smooth, VascularSignal TransductionTransforming Growth Factor betaTransforming Growth Factor betaElastin-contractile unitExtracellular matrix (ECM)Mechanosensing of SMCsSignaling pathwaysTGF-βThoracic Aortic Aneurysm (TAA)

Identifiers

PMID28943527
PMCPMC5827090
OpenAlexW2760759058

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.