Related Experiment Video
Updated: Feb 28, 2026

Murine Myocardial Infarction Model using Permanent Ligation of Left Anterior Descending Coronary Artery
Published on: August 16, 2019
Myocardial Matrix Metalloproteinase 3 Protein Expression in Ischemic Heart Failure
Vitalija Siratavičiūtė1, Dalia Pangonytė1, Vaiva Lesauskaitė1,2
1Laboratory of Cardiac Pathology, Institute of Cardiology, Lithuanian University of Health Sciences, 50162 Kaunas, Lithuania.
Abstract:
Matrix metalloproteinase 3 (MMP3), in conjunction with other MMPs, plays a key role in myocardial remodeling by breaking down the extracellular matrix of the heart and the development of heart failure (HF). However, the existing data on MMP3 protein expression in human myocardium remains insufficient. The objective of the present study was to determine the expression of MMP3 protein in left ventricular myocardial cells at varying stages of ischemic HF. To this end, a quantitative and semi-quantitative immunohistochemical analysis was performed on 113 samples of left ventricular myocardium. A non-selective digital myocardial image analysis revealed that the stage A HF group exhibited higher MMP3 protein expression compared to the control group (p < 0.001). Subsequent increases in immunostaining intensity of MMP3 were observed in the stage B HF group (p < 0.001). In the stage C/D HF group, MMP3 expression reached its highest level (p < 0.001). The intensity of immunostaining exhibited comparable tendencies in both cardiomyocytes and non-cardiomyocytes. Increased levels of MMP3 immunostaining in both types of cells were associated with increased left ventricular mass. Subjects who carried the 5A allele and patients with the 5A homozygous genotype exhibited a higher propensity for increased immunostaining levels in both cardiomyocytes and non-cardiomyocytes when compared to those with the 6A/6A and 5A/6A genotype. These changes in MMP3 protein expression were associated with left ventricular myocardial remodeling in the progression of ischemic HF.
Insights
Matrix metalloproteinase 3 (MMP3) protein expression increases with heart failure (HF) stage, contributing to myocardial remodeling. Higher MMP3 levels in cardiomyocytes and non-cardiomyocytes correlate with left ventricular mass and specific genotypes.
Area of Science:
- Cardiovascular Biology
- Molecular Cardiology
- Biochemistry
Background:
- Matrix metalloproteinase 3 (MMP3) is implicated in myocardial remodeling and heart failure (HF) pathogenesis.
- Limited data exists on MMP3 protein expression in human myocardium during HF progression.
Purpose of the Study:
- To quantify MMP3 protein expression in left ventricular myocardial cells across different stages of ischemic heart failure.
- To investigate the association between MMP3 levels, left ventricular mass, and genetic variations.
Main Methods:
- Quantitative and semi-quantitative immunohistochemical analysis of 113 left ventricular myocardial samples.
- Digital myocardial image analysis to assess MMP3 immunostaining intensity in cardiomyocytes and non-cardiomyocytes.
- Genotyping for MMP3 5A/6A polymorphism.
Main Results:
- MMP3 protein expression significantly increased from control to stage A, B, and C/D ischemic HF (p < 0.001).
- Elevated MMP3 immunostaining in both cell types correlated with increased left ventricular mass.
- The 5A allele and 5A homozygous genotype were associated with higher MMP3 expression.
Conclusions:
- MMP3 protein expression progressively increases in the human left ventricle during ischemic heart failure.
- MMP3 upregulation is linked to left ventricular myocardial remodeling and is influenced by MMP3 gene polymorphism.
Related Concept Videos
Cardiomyopathy III: Hypertrophic Cardiomyopathy
Myocarditis III: Medical Management
Myocarditis I: Introduction
Role of Matrix Metalloproteases in Degradation of ECM
Blood Studies for Cardiovascular System I: Cardiac Biomarkers
The essential diagnostic tools for detecting myocardial necrosis and monitoring individuals suspected of having acute coronary syndrome (ACS) include:
Troponins
Troponins, particularly cardiac troponins I and T, are the most precise and sensitive markers of myocardial injury. They are detectable within 4-6 hours of myocardial injury and remain...

