IMR Press / RCM / Volume 22 / Issue 2 / DOI: 10.31083/j.rcm2202059
Open Access Original Research
The pathomechanism of human myxomatous valvular degeneration at the mechanical and cellular level
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1 Department of Vascular Surgery, The First Hospital of Tsinghua University, 100016 Beijing, China
2 Department of Cardiac Surgery, The First Hospital of Tsinghua University, 100016 Beijing, China
3 Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 430022 Wuhan, Hubei, China
These authors contributed equally.
Rev. Cardiovasc. Med. 2021, 22(2), 513–519; https://doi.org/10.31083/j.rcm2202059
Submitted: 11 April 2021 | Revised: 7 May 2021 | Accepted: 11 June 2021 | Published: 30 June 2021
(This article belongs to the Special Issue State-of-the-Art Cardiovascular Medicine in Asia 2021)
Abstract

The purpose of this study was to explore the pathomechanism of human myxomatous valve degeneration by investigating changes in the phenotype of valvular cells, the metabolism of the extracellular matrix and their mechanical properties. Mitral valve specimens were harvested from patients who had undergone valve replacement, and divided into two groups: patients with a myxomatous mitral valve and a control group. Histological investigation showed that the morphology of the extracellular matrix was looser and less coordinated in myxomatous valves than in controls. α-SMA (α-smooth muscle actin) and Vimentin were positive and DNA (deoxyribonucleic acid) assay of leaflets and expression of SMemb (embryonic smooth muscle myosin heavy chain), MMP-13 (matrix Metalloproteinases-13), MMP-1 mRNA (messenger Ribonucleic Acid) of the myxomatous valves were increased while the hydroxyproline content, expression of TIMP-1 (tissue inhibitor of metalloproteinase-1) mRNA and mechanical properties were decreased compared with controls. Compared to the quiescent interstitial cells in non-myxomatous valves, interstitial cells in myxomatous valves exhibit myofibroblast activation and express excessive levels of matrix metalloproteinases. The balance between MMP/TIMP was disrupted. We conclude that overactivation of VICs (Valvular interstitial cells) and the imbalance of MMP/TIMP could be important features of the pathomechanism of myxomatous mitral valve degeneration.

Keywords
Myxomatous mitral valve
Degeneration
Valvular interstitial cell
Extracellular matrix
Mechanical property
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