Evidence map›Paper›PMID 32006823›Full record

ReviewCardiovascular pathology : the official journal of the Society for Cardiovascular Pathology

Comparative pathology of human and canine myxomatous mitral valve degeneration: 5HT and TGF-β mechanisms.

Mark A Oyama, Chad Elliott, Kerry A Loughran, Alexander P Kossar, Estibaliz Castillero, Robert J Levy, Giovanni Ferrari

Open access · greenAbstract readComparative StudyReview
In one paragraph

Review in Cardiovascular pathology : the official journal of the Society for Cardiovascular Pathology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.7field-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

45 citing papers in PubMed, 60 citations in OpenAlex.

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  18. Observational
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  20. Dynamic changes in mitral valve extracellular matrix, tissue mechanics and function in a mouse model of Marfan syndrome.Matrix biology : journal of the International Society for Matrix Biology · 2024
    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

7 authors at 4 institutions in 1 country.

Mark A OyamaDepartment of Clinical Sciences and Advanced Medicine, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA; Institute for Translational Medicine and Therapeutics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Chad ElliottDepartment of Surgery, Columbia Cardiovascular Institute and College of Physicians and Surgeons at Columbia University, New York, NY, USA.
Kerry A LoughranDepartment of Clinical Sciences and Advanced Medicine, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA, USA.
Alexander P KossarDepartment of Surgery, Columbia Cardiovascular Institute and College of Physicians and Surgeons at Columbia University, New York, NY, USA.
Estibaliz CastilleroDepartment of Surgery, Columbia Cardiovascular Institute and College of Physicians and Surgeons at Columbia University, New York, NY, USA.
Robert J LevyThe Children's Hospital of Philadelphia, Philadelphia, PA, USA.
Giovanni FerrariDepartment of Surgery, Columbia Cardiovascular Institute and College of Physicians and Surgeons at Columbia University, New York, NY, USA. Electronic address: gf2375@cumc.columbia.edu.
Columbia University · USChildren's Hospital of Philadelphia · USTranslational Therapeutics (United States) · USUniversity of Pennsylvania · US

Funding

POSTDOCTORAL TRAINING IN CARDIOVASCULAR DISEASET32HL007854 · NHLBI · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Marwah Abdalla, Michael Argenziano · 1996 to 2026
$14.7M
Supplement to Serotonin Signaling in Mitral Valve Homeostasis, Maintenance and RestorationR01HL131872 · NHLBI · CHILDREN'S HOSP OF PHILADELPHIA · PI Giovanni Ferrari, Robert J Levy · 2016 to 2026
$7.7M
Role of RAGE in Bicuspid Aortic Valve SyndromeR01HL122805 · NHLBI · UNIVERSITY OF PENNSYLVANIA · PI FERRARI, GIOVANNI · 2016 to 2019
$1.6M
NHLBI NIH HHS R01 HL122805NHLBI NIH HHS R01 HL131872NHLBI NIH HHS T32 HL007854
6 · The paper itself

Abstract

Myxomatous mitral valve degeneration (MMVD) is a leading cause of valve repair or replacement secondary to the production of mitral regurgitation, cardiac enlargement, systolic dysfunction, and heart failure. The pathophysiology of myxomatous mitral valve degeneration is complex and incompletely understood, but key features include activation and transformation of mitral valve (MV) valvular interstitial cells (VICs) into an active phenotype leading to remodeling of the extracellular matrix and compromise of the structural components of the mitral valve leaflets. Uncovering the mechanisms behind these events offers the potential for therapies to prevent, delay, or reverse myxomatous mitral valve degeneration. One such mechanism involves the neurotransmitter serotonin (5HT), which has been linked to development of valvulopathy in a variety of settings, including valvulopathy induced by serotonergic drugs, Serotonin-producing carcinoid tumors, and development of valvulopathy in laboratory animals exposed to high levels of serotonin. Similar to humans, the domestic dog also experiences naturally occurring myxomatous mitral valve degeneration, and in some breeds of dogs, the lifetime prevalence of myxomatous mitral valve degeneration reaches 100%. In dogs, myxomatous mitral valve degeneration has been associated with high serum serotonin, increased expression of serotonin-receptors, autocrine production of serotonin within the mitral valve leaflets, and downregulation of serotonin clearance mechanisms. One pathway closely associated with serotonin involves transforming growth factor beta (TGF-β) and the two pathways share a common ability to activate mitral valve valvular interstitial cells in both humans and dogs. Understanding the role of serotonin and transforming growth factor beta in myxomatous mitral valve degeneration gives rise to potential therapies, such as 5HT receptor (5HT-R) antagonists. The main purposes of this review are to highlight the commonalities between myxomatous mitral valve degeneration in humans and dogs, with specific regards to serotonin and transforming growth factor beta, and to champion the dog as a relevant and particularly valuable model of human disease that can accelerate development of novel therapies.

Indexed as

AnimalsDog DiseasesDogsHumansMitral ValveMitral Valve InsufficiencyMitral Valve ProlapseSerotoninSignal TransductionSpecies SpecificityTransforming Growth Factor betaSerotoninTransforming Growth Factor betaMitral valve diseaseMitral valve repairMitral valve replacementMyxomatous mitral valve degenerationSerotonin

Identifiers

PMID32006823
PMCPMC7078050
OpenAlexW3000537087

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.