Evidence map›Paper›PMID 26963838›Full record

ArticleJournal of biomechanical engineering2016

Reduced Biaxial Contractility in the Descending Thoracic Aorta of Fibulin-5 Deficient Mice.

S-I Murtada, J Ferruzzi, H Yanagisawa, J D Humphrey

Open access · bronzeAbstract read
In one paragraph

Article in Journal of biomechanical engineering, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.5field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 38 citations in OpenAlex.

  1. Biomechanical function of the murine cervix with elastic fiber deficiency.Journal of the mechanical behavior of biomedical materials · 2026
    Article
  2. Endothelial cell (EC)-specific Ctgf/Ccn2 expression increases EC reprogramming and atherosclerosis.Matrix biology : journal of the International Society for Matrix Biology · 2025
    Article
  3. Article
  4. Smooth muscle contribution to vaginal viscoelastic response.Journal of the mechanical behavior of biomedical materials · 2023
    Article
  5. Compromised Cardiopulmonary Function in Fibulin-5 Deficient Mice.Journal of biomechanical engineering · 2022
    Article
  6. Biaxial Murine Vaginal Remodeling With Reproductive Aging.Journal of biomechanical engineering · 2022
    Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Developmental origins of mechanical homeostasis in the aorta.Developmental dynamics : an official publication of the American Association of Anatomists · 2021
    Article
  13. Article
  14. Article
  15. [Experimental measurement and modeling analysis of active and passive mechanical properties of arterial vessel wall].Sheng wu yi xue gong cheng xue za zhi = Journal of biomedical engineering = Shengwu yixue gongchengxue zazhi · 2020
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Elastic fibers and biomechanics of the aorta: Insights from mouse studies.Matrix biology : journal of the International Society for Matrix Biology · 2020
    Review
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

4 authors at 3 institutions in 3 countries.

S-I Murtada
J Ferruzzi
H Yanagisawa
J D Humphrey
Yale University · USKarolinska Institutet · SEUniversity of Tsukuba · JP

Funding

Mechanisms Underlying The Progression of Large Artery Stiffness in HypertensionR01HL105297 · NHLBI · YALE UNIVERSITY · PI FIGUEROA, CARLOS ALBERTO, HUMPHREY, JAY D. · 2010 to 2019
$3.0M
NHLBI NIH HHS R01 HL105297
6 · The paper itself

Abstract

The precise role of smooth muscle cell contractility in elastic arteries remains unclear, but accumulating evidence suggests that smooth muscle dysfunction plays an important role in the development of thoracic aortic aneurysms and dissections (TAADs). Given the increasing availability of mouse models of these conditions, there is a special opportunity to study roles of contractility ex vivo in intact vessels subjected to different mechanical loads. In parallel, of course, there is a similar need to study smooth muscle contractility in models that do not predispose to TAADs, particularly in cases where disease might be expected. Multiple mouse models having compromised glycoproteins that normally associate with elastin to form medial elastic fibers present with TAADs, yet those with fibulin-5 deficiency do not. In this paper, we show that deletion of the fibulin-5 gene results in a significantly diminished contractility of the thoracic aorta in response to potassium loading despite otherwise preserved characteristic active behaviors, including axial force generation and rates of contraction and relaxation. Interestingly, this diminished response manifests around an altered passive state that is defined primarily by a reduced in vivo axial stretch. Given this significant coupling between passive and active properties, a lack of significant changes in passive material stiffness may help to offset the diminished contractility and thereby protect the wall from detrimental mechanosensing and its sequelae.

Indexed as

VasoconstrictionAnimalsAorta, ThoracicExtracellular Matrix ProteinsGenotypeMaleMiceRecombinant ProteinsStress, MechanicalExtracellular Matrix ProteinsFbln5 protein, mouseRecombinant Proteins

Identifiers

PMID26963838
PMCPMC4843850
OpenAlexW2301386507

What OpenQuestion holds

Textmetadata
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.