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Reviews in Cardiovascular Medicine  2021, Vol. 22 Issue (2): 513-519     DOI: 10.31083/j.rcm2202059
Special Issue: State-of-the-Art Cardiovascular Medicine in Asia 2021
Original Research Previous articles | Next articles
The pathomechanism of human myxomatous valvular degeneration at the mechanical and cellular level
Chang Hu1, †, Qian Wang1, †, Hui Xue2, Hao Hong3, Jiawei Shi3, Nianguo Dong3, *(), Mingkui Zhang2, *()
1Department of Vascular Surgery, The First Hospital of Tsinghua University, 100016 Beijing, China
2Department of Cardiac Surgery, The First Hospital of Tsinghua University, 100016 Beijing, China
3Department of Cardiovascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, 430022 Wuhan, Hubei, China
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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.
Key words:  Myxomatous mitral valve      Degeneration      Valvular interstitial cell      Extracellular matrix      Mechanical property     
Submitted:  11 April 2021      Revised:  07 May 2021      Accepted:  11 June 2021      Published:  30 June 2021     
2016YFA0101100/National Key Research and Development Program of China
81930052/National Natural Science Foundation of China
20161080069/Tsinghua University Initiative Scientific Research Program
LH-03/Pilot Fund of the The First Hospital of Tsinghua University
*Corresponding Author(s): (Nianguo Dong); (Mingkui Zhang)   
About author:  These authors contributed equally.

Cite this article: 

Chang Hu, Qian Wang, Hui Xue, Hao Hong, Jiawei Shi, Nianguo Dong, Mingkui Zhang. The pathomechanism of human myxomatous valvular degeneration at the mechanical and cellular level. Reviews in Cardiovascular Medicine, 2021, 22(2): 513-519.

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