Evidence map›Paper›PMID 27406839›Full record

ReviewHeart (British Cardiac Society)2016

Cell-matrix mechanics and pattern formation in inflammatory cardiovascular calcification.

Jeffrey J Hsu, Jina Lim, Yin Tintut, Linda L Demer

Open access · greenAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Heart (British Cardiac Society), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
4.8field-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

27 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Collagen VIII in vascular diseases.Matrix biology : journal of the International Society for Matrix Biology · 2024
    Review
  5. Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. The Role of Inflammation in Cardiovascular Disease.International journal of molecular sciences · 2022
    Review
  11. Article
  12. Skeleton-secreted PDGF-BB mediates arterial stiffening.The Journal of clinical investigation · 2021
    Article
  13. Changes in microarchitecture of atherosclerotic calcification assessed byJournal of nuclear cardiology : official publication of the American Society of Nuclear Cardiology · 2021
    Article
  14. Article
  15. A narrative review of exosomes in vascular calcification.Annals of translational medicine · 2021
    Review
  16. Article
  17. The Matrisome, Inflammation, and Liver Disease.Seminars in liver disease · 2020
    Review
  18. Coronary Atherosclerosis Imaging.Diagnostics (Basel, Switzerland) · 2020
    Review
  19. Article
  20. 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 2 institutions in 1 country.

Jeffrey J HsuDepartment of Medicine, Division of Cardiology, University of California, Los Angeles (UCLA), Los Angeles, California, USA.
Jina LimDepartment of Pediatrics, University of California, Los Angeles (UCLA), Los Angeles, California, USA.
Yin TintutDepartment of Medicine, Division of Cardiology, University of California, Los Angeles (UCLA), Los Angeles, California, USA Department of Physiology, University of California, Los Angeles (UCLA), Los Angeles, California, USA Department of Orthopaedic Surgery, University of California, Los Angeles (UCLA), Los Angeles, California, USA.
Linda L DemerDepartment of Medicine, Division of Cardiology, University of California, Los Angeles (UCLA), Los Angeles, California, USA Department of Physiology, University of California, Los Angeles (UCLA), Los Angeles, California, USA Department of Bioengineering, University of California, Los Angeles (UCLA), Los Angeles, California, USA.
University of California, Los Angeles · USOklahoma State University Center for Health Sciences · US

Funding

CARDIOVASCULAR SCIENTIST TRAINING PROGRAMT32HL007895 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI SHIVKUMAR, KALYANAM, WATSON, KAROL E · 1998 to 2023
$9.2M
Mechanisms of intermittent parathyroid hormone effects on calcific aortic diseaseR01HL121019 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEMER, LINDA L., TINTUT, YIN · 2015 to 2018
$1.5M
Role of Inhibitory SMADs in Calcific Aortic Valve DiseaseR01HL114709 · NHLBI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DEMER, LINDA L., TINTUT, YIN · 2012 to 2015
$1.5M
NHLBI NIH HHS R01 HL114709NHLBI NIH HHS R01 HL121019NHLBI NIH HHS T32 HL007895
6 · The paper itself

Abstract

Calcific diseases of the cardiovascular system, such as atherosclerotic calcification and calcific aortic valve disease, are widespread and clinically significant, causing substantial morbidity and mortality. Vascular cells, like bone cells, interact with their matrix substrate through molecular signals, and through biomechanical signals, such as traction forces transmitted from cytoskeleton to matrix. The interaction of contractile vascular cells with their matrix may be one of the most important factors controlling pathological mineralisation of the artery wall and cardiac valves. In many respects, the matricrine and matrix mechanical changes in calcific vasculopathy and valvulopathy resemble those occurring in embryonic bone development and normal bone mineralisation. The matrix proteins provide a microenvironment for propagation of crystal growth and provide mechanical cues to the cells that direct differentiation. Small contractions of the cytoskeleton may tug on integrin links to sites on matrix proteins, and thereby sense the stiffness, possibly through deformation of binding proteins causing release of differentiation factors such as products of the members of the transforming growth factor-β superfamily. Inflammation and matrix characteristics are intertwined: inflammation alters the matrix such as through matrix metalloproteinases, while matrix mechanical properties affect cellular sensitivity to inflammatory cytokines. The adhesive properties of the matrix also regulate self-organisation of vascular cells into patterns through reaction-diffusion phenomena and left-right chirality. In this review, we summarise the roles of extracellular matrix proteins and biomechanics in the development of inflammatory cardiovascular calcification.

Indexed as

Mechanotransduction, CellularAnimalsAortic ValveAortic Valve StenosisArteriesAtherosclerosisBiomechanical PhenomenaCalcinosisCell AdhesionCellular MicroenvironmentCytokinesElasticityExtracellular MatrixFeedback, PhysiologicalHumansInflammationCytokinesInflammation Mediators

Identifiers

PMID27406839
PMCPMC5069068
OpenAlexW2467529093

What OpenQuestion 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 OpenQuestion graph.