Role of matrix metalloproteinases in mitral valve regurgitation: Association between the of MMP-1, MMP-9, TIMP-1, and TIMP-2 expression, degree of mitral valve insufficiency, and pathologic etiology.


Journal

Journal of cardiac surgery
ISSN: 1540-8191
Titre abrégé: J Card Surg
Pays: United States
ID NLM: 8908809

Informations de publication

Date de publication:
Jun 2022
Historique:
revised: 07 02 2022
received: 19 01 2022
accepted: 02 03 2022
pubmed: 29 3 2022
medline: 21 4 2022
entrez: 28 3 2022
Statut: ppublish

Résumé

The pathogenesis of mitral valve insufficiency is not yet fully understood. Several studies stressed the role of matrix metalloproteinases (MMPs) in the emergence of valvular pathologies. The primary objective of the present study is to analyze the role of selected MMPs and their inhibitors in mitral valve insufficiency. Eighty patients (33 female/47 male, mean age 67 years) underwent cardiopulmonary bypass surgery for mitral valve reconstruction between 2007 and 2015. All patients suffered from mitral insufficiency (MI) Stages iii and iv. When tissue resection was acquired specimens were taken immediately frozen and used for histological examination. Expression of MMP-1, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-1, and TIMP-2 was examined immunohistochemically and distribution was analyzed in regard to preoperative clinical, echocardiographic, and histopathological findings. A clear correlation between the MMP expression and the MI degree of severity could be shown. The expression of MMPs proved to be high in relation to mild insufficiencies and relatively weak in the case of severe ones. Additionally, the etiology of the MI was considered in the analysis and a significant difference in the expression of MMPs between the mitral valves with endocarditis and the ones featuring a degenerative disease could be shown. Within the group of valves with degenerative diseases, no significant difference could be established between the subgroups (myxoid and sclerosed valves). The increased expression of MMPs and their inhibitors in mild insufficiencies could prove that the molecular changes in the valve precede the macroscopical and thus the echocardiographically diagnosable changes. Hence, new options for early diagnosis and therapy of MIs should be examined in further studies, respectively. Herein, the correlation of the MMP blood levels with MMP tissue expression should be addressed for surgical therapeutical decisions.

Sections du résumé

BACKGROUND BACKGROUND
The pathogenesis of mitral valve insufficiency is not yet fully understood. Several studies stressed the role of matrix metalloproteinases (MMPs) in the emergence of valvular pathologies. The primary objective of the present study is to analyze the role of selected MMPs and their inhibitors in mitral valve insufficiency.
PATIENTS AND METHODS METHODS
Eighty patients (33 female/47 male, mean age 67 years) underwent cardiopulmonary bypass surgery for mitral valve reconstruction between 2007 and 2015. All patients suffered from mitral insufficiency (MI) Stages iii and iv. When tissue resection was acquired specimens were taken immediately frozen and used for histological examination. Expression of MMP-1, MMP-9, tissue inhibitor of metalloproteinase (TIMP)-1, and TIMP-2 was examined immunohistochemically and distribution was analyzed in regard to preoperative clinical, echocardiographic, and histopathological findings.
RESULTS RESULTS
A clear correlation between the MMP expression and the MI degree of severity could be shown. The expression of MMPs proved to be high in relation to mild insufficiencies and relatively weak in the case of severe ones. Additionally, the etiology of the MI was considered in the analysis and a significant difference in the expression of MMPs between the mitral valves with endocarditis and the ones featuring a degenerative disease could be shown. Within the group of valves with degenerative diseases, no significant difference could be established between the subgroups (myxoid and sclerosed valves).
CONCLUSION CONCLUSIONS
The increased expression of MMPs and their inhibitors in mild insufficiencies could prove that the molecular changes in the valve precede the macroscopical and thus the echocardiographically diagnosable changes. Hence, new options for early diagnosis and therapy of MIs should be examined in further studies, respectively. Herein, the correlation of the MMP blood levels with MMP tissue expression should be addressed for surgical therapeutical decisions.

Identifiants

pubmed: 35343608
doi: 10.1111/jocs.16449
doi:

Substances chimiques

Tissue Inhibitor of Metalloproteinase-1 0
Tissue Inhibitor of Metalloproteinases 0
Tissue Inhibitor of Metalloproteinase-2 127497-59-0
Matrix Metalloproteinases EC 3.4.24.-
Matrix Metalloproteinase 9 EC 3.4.24.35
Matrix Metalloproteinase 1 EC 3.4.24.7

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1613-1622

Commentaires et corrections

Type : CommentIn

Informations de copyright

© 2022 The Authors. Journal of Cardiac Surgery published by Wiley Periodicals LLC.

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Auteurs

Marc Irqsusi (M)

Department of Cardiovascular Surgery, University Hospital Gießen and Marburg, Marburg, Germany.

Azza Labene Mansouri (AL)

Department of Cardiovascular Surgery, University Hospital Gießen and Marburg, Marburg, Germany.

Anette Ramaswamy (A)

Institute for Pathology, University Hospital Gießen and Marburg, Marburg, Germany.

Peter Rexin (P)

Institute for Pathology, University Hospital Gießen and Marburg, Marburg, Germany.

Midhat Salman (M)

Department of Forensic Sciences, University of Health Sciences, Lahore, Pakistan.

Saqib Mahmood (S)

Department of Human Genetics and Molecular Biology, University of Health Sciences, Lahore, Pakistan.

Nikolas Mirow (N)

Department of Cardiovascular Surgery, University Hospital Gießen and Marburg, Marburg, Germany.

Tamer Ghazi (T)

Department of Cardiovascular Surgery, University Hospital Gießen and Marburg, Marburg, Germany.

Rabia Ramzan (R)

Department of Cardiovascular Surgery, University Hospital Gießen and Marburg, Marburg, Germany.

Ardawan J Rastan (AJ)

Department of Cardiovascular Surgery, University Hospital Gießen and Marburg, Marburg, Germany.

Sebastian Vogt (S)

Department of Cardiovascular Surgery, University Hospital Gießen and Marburg, Marburg, Germany.

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