Evidence map›Paper›PMID 29054843›Full record

ArticleJournal of the American Heart Association2017

Contribution of Extra-Cardiac Cells in Murine Heart Valves is Age-Dependent.

Lindsey J Anstine, Tori E Horne, Edwin M Horwitz, Joy Lincoln

Open access · goldAbstract readComparative Study
In one paragraph

Article in Journal of the American Heart Association, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
4.3field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 61 citations in OpenAlex.

  1. Article
  2. Unveiling the intricacies of cardiac valve pathophysiology.Frontiers in cardiovascular medicine · 2025
    Review
  3. Review
  4. WGCNA and molecular docking identify hub genes for cardiac aging.Frontiers in cardiovascular medicine · 2023
    Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. The Endocardium and Heart Valves.Cold Spring Harbor perspectives in biology · 2020
    Review
  10. Article
  11. New Concepts in the Development and Malformation of the Arterial Valves.Journal of cardiovascular development and disease · 2020
    Review
  12. Macrophages Promote Aortic Valve Cell Calcification and Alter STAT3 Splicing.Arteriosclerosis, thrombosis, and vascular biology · 2020
    Article
  13. Adaptive immune cells in calcific aortic valve disease.American journal of physiology. Heart and circulatory physiology · 2019
    Review
  14. Article
  15. Review
  16. Article
  17. Review
  18. Article
  19. Article
  20. Significance of inflammation-related markers and histopathological features in mitral valve regurgitation.Romanian journal of morphology and embryology = Revue roumaine de morphologie et embryologie
    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

4 authors at 2 institutions in 1 country.

Lindsey J AnstineMolecular, Cellular and Developmental Biology Graduate Program, The Ohio State University, Columbus, OH.
Tori E HorneCenter for Cardiovascular Research, The Research Institute at Nationwide Children's Hospital, Columbus, OH.
Edwin M HorwitzDepartment of Pediatrics, The Ohio State University, Columbus, OH.
Joy LincolnDepartment of Pediatrics, The Ohio State University, Columbus, OH joy.lincoln@nationwidechildrens.org.
Nationwide Children's Hospital · USThe Ohio State University · US

Funding

The Role of Sox9 in Calcific Aortic Valve DiseaseR01HL127033 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI LINCOLN, JOY · 2015 to 2018
$1.5M
NHLBI NIH HHS R01 HL127033
6 · The paper itself

Abstract

backgroundHeart valves are dynamic structures that open and close over 100 000 times a day to maintain unidirectional blood flow during the cardiac cycle. Function is largely achieved by highly organized layers of extracellular matrix that provide the necessary biomechanical properties. Homeostasis of valve extracellular matrix is mediated by valve endothelial and interstitial cell populations, and although the embryonic origins of these cells are known, it is not clear how they are maintained after birth. The goal of this study is to examine the contribution of extracardiac cells to the aortic valve structure with aging using lineage tracing and bone marrow transplantation approaches. METHODS AND

resultsImmunohistochemistry and fate mapping studies using

conclusionsFindings from this study demonstrate that the percentage of CD45-positive extracardiac cells reside within endothelial and interstitial regions of heart valve structures increases with age. In addition, bone transplantation studies show that engraftment is dependent on the age of the donor and age of the tissue environment of the recipient. These studies create a foundation for further work defining the role of extracardiac cells in homeostatic and diseased heart valves.

Indexed as

Cell LineageAge FactorsAgingAnimalsAortic ValveBiomarkersBone Marrow TransplantationCD11b AntigenCell DifferentiationCell SurvivalEndothelial CellsGreen Fluorescent ProteinsHematopoietic Stem CellsIntegrasesLeukocyte Common AntigensMice, Inbred C57BLBiomarkersCD11b AntigenCre recombinaseenhanced green fluorescent proteinGreen Fluorescent ProteinsIntegrasesLeukocyte Common AntigensPlatelet Endothelial Cell Adhesion Molecule-1PTPRC protein, humanVimentinbone marrow transplantextra cardiacheart valveheart valve endothelial cellheart valve interstitial cell

Identifiers

PMID29054843
PMCPMC5721893
OpenAlexW2766846776

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.