Evidence map›Paper›PMID 38185344›Full record

ArticleMatrix biology : journal of the International Society for Matrix Biology2024

Dynamic changes in mitral valve extracellular matrix, tissue mechanics and function in a mouse model of Marfan syndrome.

Brittany A Gonzalez, Samuel W Harmeyer, Taejeong Song, Sakthivel Sadayappan, Katherine E Yutzey

Open access · greenAbstract read
In one paragraph

Article in Matrix biology : journal of the International Society for Matrix Biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
3.3field-weighted citation impact, top 9% 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

7 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Immune Mechanisms of Heart Valve Development, Homeostasis, and Disease.Arteriosclerosis, thrombosis, and vascular biology · 2026
    Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. 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

5 authors at 2 institutions in 1 country.

Brittany A GonzalezThe Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Samuel W HarmeyerThe Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA.
Taejeong SongInternal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Sakthivel SadayappanInternal Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA.
Katherine E YutzeyThe Heart Institute, Division of Molecular Cardiovascular Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH, USA; Department of Pediatrics, University of Cincinnati College of Medicine, Cincinnati OH, USA. Electronic address: Katherine.Yutzey@cchmc.org.
Cincinnati Children's Hospital Medical Center · USUniversity of Cincinnati Medical Center · US

Funding

Understanding Cardiovascular Disease MechanismsT32HL125204 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI Evangelia G Kranias, Jeffery D Molkentin · 2015 to 2026
$3.4M
Mechanisms of Congenital Heart Valve DiseaseR01HL143881 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI YUTZEY, KATHERINE E · 2018 to 2021
$1.9M
Endothelial subpopulations in heart valve development and congenital heart diseaseR01HL156270 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI YUTZEY, KATHERINE E · 2021 to 2024
$1.9M
The role of dendritic cells in heart valve extracellular matrix remodeling, homeostasis, and diseaseF32HL168787 · NHLBI · CINCINNATI CHILDRENS HOSP MED CTR · PI GONZALEZ, BRITTANY A. · 2023 to 2023
$17k
American Heart Association-American Stroke Association 23POST1019132National Institutes of Health (NIH) Heart, Lung and Blood Institute 1F32HL168787-01NHLBI NIH HHS F32 HL168787NHLBI NIH HHS R01 HL143881NHLBI NIH HHS R01 HL156270NHLBI NIH HHS T32 HL125204
6 · The paper itself

Abstract

objectiveMouse models of Marfan syndrome (MFS) with Fibrillin 1 (Fbn1) variant C1041G exhibit cardiovascular abnormalities, including myxomatous valve disease (MVD) and aortic aneurism, with structural extracellular matrix (ECM) dysregulation. In this study, we examine the structure-function-mechanics relations of the mitral valve related to specific transitions in ECM composition and organization in progressive MVD in MFS mice from Postnatal day (P)7 to 1 year-of-age. APPROACH AND

resultsMechanistic links between mechanical forces and biological changes in MVD progression were examined in Fbn1

conclusionsAltogether, our data indicate dynamic regulation of mitral valve structure, tissue mechanics, and function that reflect changes in ECM composition, organization, and gene expression in progressive MVD. Notably, increased collagen fiber organization and orientation, potentially dependent on increased matrifibrocyte cell activity, is apparent with altered mitral valve mechanics and function in aging MFS mice.

Indexed as

Marfan SyndromeAnimalsCollagenExtracellular MatrixFibrillin-1MiceMitral ValveProteoglycansCollagenFibrillin-1ProteoglycansCollagen organization and structureMyxomatous mitral valveProteoglycansValve functionValve tissue stiffness

Identifiers

PMID38185344
PMCPMC12034306
OpenAlexW4390630328

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.