Matrix metalloproteinases: not-so-innocent bystanders in heart failure
Key result
Overexpression of human MMP-1 in the cardiac ventricles of mice disrupts the extracellular matrix, leading to myocyte hypertrophy by 6 months and systolic and diastolic dysfunction by 12 months.
Design
Editorial
Authors
Discussion
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Implication
Highlights the emerging role of the extracellular matrix and matrix metalloproteinases in the pathophysiology of heart failure, challenging the traditional myocyte-centric view.
PICO
P
Population
Heart failure
I
Intervention / Comparator
MMP-1 overexpression
Highlights the emerging role of the extracellular matrix and matrix metalloproteinases in the pathophysiology of heart failure, challenging the traditional myocyte-centric view.
Limitations
- The discussed transgenic mouse model is an artificial system.
- Collagen degradation is unlikely to be the usual initiating factor for human heart failure.
Cite This Study
Lee et al. (2000) conducted an editorial in Heart failure. MMP-1 overexpression was evaluated. Overexpression of human MMP-1 in the cardiac ventricles of mice disrupts the extracellular matrix, leading to myocyte hypertrophy by 6 months and systolic and diastolic dysfunction by 12 months.