SynthesisFrontiers in cardiovascular medicine2022
The Role of Transforming Growth Factor-β Signaling in Myxomatous Mitral Valve Degeneration.
Synthesis in Frontiers in cardiovascular medicine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 25 citations in OpenAlex.
- Mechanisms of mitral valve development and disease.Frontiers in cardiovascular medicine · 2026Review
- BMPR2 affects valve development via ECM-receptor interaction in zebrafish.Frontiers in cell and developmental biology · 2026Article
- Dapagliflozin inhibits TGF-β-induced transdifferentiation of valvular interstitial cells and mitral valvular degeneration.Journal of molecular medicine (Berlin, Germany) · 2025Article
- Genetic Basis of Myxomatous Mitral Valve Disease in Cavalier King Charles Spaniel Dogs-A Review.Veterinary sciences · 2025Review
- Aged Zebrafish as a Spontaneous Model of Cardiac Valvular Disease.Aging cell · 2025Article
- Long-Term Surgical Outcome for Idiopathic Acute Rupture of Mitral Chordae Tendineae in Infants.Interdisciplinary cardiovascular and thoracic surgery · 2025Article
- Cardiology's best friend: Using naturally occurring disease in dogs to understand heart disease in humans.Journal of molecular and cellular cardiology plus · 2025Review
- Genotype-Phenotype Correlations, Treatment, and Prognosis of Children With Early-Onset (Neonatal) Marfan Syndrome.Clinical genetics · 2025Article
- Involvement of TGF-β, mTOR, and inflammatory mediators in aging alterations during myxomatous mitral valve disease in a canine model.GeroScience · 2025Review
- Article
- Hemodynamic forces prevent myxomatous valve disease in mice through KLF2/4 signaling.The Journal of clinical investigation · 2025Article
- Single-cell analysis reveals the loss of FABP4-positive proliferating valvular endothelial cells relates to functional mitral regurgitation.BMC medicine · 2024Article
- Mitral Annular Disjunction in Heritable Thoracic Aortic Disease: Insights From the Montalcino Aortic Consortium.Journal of the American Heart Association · 2024Article
- Review
- Mitral valve transcriptome analysis in thirty-four age-matched Cavalier King Charles Spaniels with or without congestive heart failure caused by myxomatous mitral valve disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2024Article
- Epicardial deletion of Sox9 leads to myxomatous valve degeneration and identifies Cd109 as a novel gene associated with valve development.Journal of molecular and cellular cardiology · 2024Article
- Article
- Genetics and pathophysiology of mitral valve prolapse.Frontiers in cardiovascular medicine · 2023Review
- Pro-Inflammatory and Immunological Profile of Dogs with Myxomatous Mitral Valve Disease.Veterinary sciences · 2022Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitral valve prolapse (MVP) due to myxomatous degeneration is one of the most important chronic degenerative cardiovascular diseases in people and dogs. It is a common cause of heart failure leading to significant morbidity and mortality in both species. Human MVP is usually classified into primary or non-syndromic, including Barlow's Disease (BD), fibro-elastic deficiency (FED) and Filamin-A mutation, and secondary or syndromic forms (typically familial), such as Marfan syndrome (MFS), Ehlers-Danlos syndrome, and Loeys-Dietz syndrome. Despite different etiologies the diseased valves share pathological features consistent with myxomatous degeneration. To reflect this common pathology the condition is often called myxomatous mitral valve degeneration (disease) (MMVD) and this term is universally used to describe the analogous condition in the dog. MMVD in both species is characterized by leaflet thickening and deformity, disorganized extracellular matrix, increased transformation of the quiescent valve interstitial cell (qVICs) to an activated state (aVICs), also known as activated myofibroblasts. Significant alterations in these cellular activities contribute to the initiation and progression of MMVD due to the increased expression of transforming growth factor-β (TGF-β) superfamily cytokines and the dysregulation of the TGF-β signaling pathways. Further understanding the molecular mechanisms of MMVD is needed to identify pharmacological manipulation strategies of the signaling pathway that might regulate VIC differentiation and so control the disease onset and development. This review briefly summarizes current understanding of the histopathology, cellular activities, molecular mechanisms and pathogenesis of MMVD in dogs and humans, and in more detail reviews the evidence for the role of TGF-β.
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