Evidence map›Paper›PMID 32824919›Full record

ArticleJournal of cardiovascular development and disease2020

Smooth Muscle α-Actin Expression in Mitral Valve Interstitial Cells is Important for Mediating Extracellular Matrix Remodeling.

Bailey K Dye, Catalina Butler, Joy Lincoln

Open access · goldAbstract read
In one paragraph

Article in Journal of cardiovascular development and disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.2field-weighted citation impact, top 18% 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

10 citing papers in PubMed, 9 citations in OpenAlex.

  1. Article
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  9. Review
  10. Biology and Biomechanics of the Heart Valve Extracellular Matrix.Journal of cardiovascular development and disease · 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

3 authors at 1 institution in 1 country.

Bailey K DyeBiomedical Sciences Graduate Program, The Ohio State University, Columbus, OH 43217, USA.
Catalina ButlerHarvard College, Boston, MA 02138, USA.ORCID 0000-0002-0096-0197
Joy LincolnDepartment of Pediatrics, Medical College of Wisconsin, Milwaukee, WI 53226, USA.ORCID 0000-0003-1517-6888
Children's Hospital of Wisconsin · US

Funding

Medical Therapies in the Treatment of Calcific Aortic Valve DiseaseR01HL142685 · NHLBI · RESEARCH INST NATIONWIDE CHILDREN'S HOSP · PI LINCOLN, JOY · 2018 to 2022
$2.2M
Advancing a Healthier Wisconsin N/AAmerican Heart Association 17UFEL33420025NHLBI NIH HHS HL142685NHLBI NIH HHS R01 HL142685The Ohio State University Presidential Fellowship N/A
6 · The paper itself

Abstract

backgroundMitral valve prolapse (MVP) affects 3-6% of the total population including those with connective tissue disorders. Treatment is limited, and patients commonly require surgery which can be impermanent and insuperable. Abnormal prolapse of mitral valve leaflets into the left atria is caused by disturbances to the composition and organization of the extracellular matrix (ECM), that weaken biomechanics. This process, known as myxomatous degeneration is characterized by an abnormal accumulation of proteoglycans, in addition to collagen fiber disruption and elastic fiber fragmentation. The underlying mechanisms that promote myxomatous degeneration to the point of biomechanical failure are unknown, but previous histological studies of end-stage diseased tissue have reported abnormal α-smooth muscle actin (SMA) in a subset of heart valve interstitial cells (VICs); however, the contribution of these abnormal cells to MVP pathogenesis has not been extensively examined.

methodsIn vivo and in vitro approaches were used. Mice harboring a

resultsWe show, in mitral valves from

conclusionsTogether, our data show that in VICs, SMA, an actin binding protein, is important for mediating ECM remodeling associated with phenotypes observed in myxomatous degeneration, and its expression is regulated by mechanical tension. These novel insights could inform the development of future non-surgical therapeutics to halt the progression of mitral valve degeneration thereby avoiding end-stage prolapse.

Indexed as

extracellular matrixheart valveheart valve interstitial cellsmyxomatous degeneration

Identifiers

PMID32824919
PMCPMC7570306
OpenAlexW3069375483

What OpenQuestion holds

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LicenceCC BY
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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.