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Role of extracellular matrix proteins in heart function
V Pelouch1, I M Dixon, L Golfman
1Division of Cardiovascular Sciences, St. Boniface General Hospital Research Centre, Faculty of Medicine, University of Manitoba, Winnipeg, Canada.
Insights
The cardiac extracellular matrix, composed mainly of collagen, dynamically changes, impacting heart function. Its alterations are linked to cardiovascular diseases like hypertension and heart failure.
Area of Science:
- Cardiovascular Biology
- Extracellular Matrix Research
- Cardiac Pathophysiology
Background:
- The cardiac interstitium contains fibroblasts and endothelial cells that produce extracellular matrix (ECM).
- ECM alterations are implicated in cardiovascular complications such as diabetes, hypertension, cardiac hypertrophy, and heart failure.
- The renin-angiotensin-aldosterone system plays a role in abnormal ECM deposition during cardiac hypertrophy and failure.
Purpose of the Study:
- To explore the dynamic nature of the cardiac extracellular matrix.
- To understand the mechanisms driving fibroblast and endothelial cell activation.
- To elucidate the role of ECM changes in heart dysfunction.
Main Methods:
- Literature review of existing data on cardiac interstitium and ECM.
- Analysis of studies investigating fibroblast and endothelial cell activation.
- Examination of the impact of aging, hypoxia, and nutrition on cardiac ECM.
Main Results:
- Cardiac ECM is primarily composed of collagen types I and III, forming fibrils that support myocardial structure.
- ECM is a dynamic entity, with alterations contributing to heart dysfunction.
- The renin-angiotensin-aldosterone system is involved in ECM deposition in pathological cardiac hypertrophy and failure.
Conclusions:
- Alterations in the cardiac extracellular matrix are integral to the development of heart dysfunction.
- Understanding ECM dynamics is crucial for addressing cardiovascular diseases.
- Further research into fibroblast and endothelial cell activation mechanisms is warranted.
Abstract:
The cardiac interstitium is populated by nonmyocyte cell types including transcriptionally active cardiac fibroblasts and endothelial cells. Since these cells are the source of many components of the cardiac extracellular matrix, and because changes in cardiac extracellular matrix are suspected of contributing to the genesis of cardiovascular complications in disease states such as diabetes, hypertension, cardiac hypertrophy and congestive heart failure, interest in the mechanisms of activation of fibroblasts and endothelial cells has led to progress in understanding these processes. Recent work provides evidence for the role of the renin-angiotensin-aldosterone system in the pathogenesis of abnormal deposition of extracellular matrix in the cardiac interstitium during the development of inappropriate cardiac hypertrophy and failure. The cardiac extracellular matrix is also known to change in response to altered cardiac performance associated with post-natal aging, and in response to environmental stimuli including intermittent hypoxia and abnormal nutrition. It is becoming clear that the extracellular matrix mainly consists of molecules of collagen types I and III; they form fibrils and provide most of the connective material for typing together myocytes and other structures in the myocardium and thus is involved in the transmission of developed mechanical force. The data available in the literature support the view that the extracellular matrix is a dynamic entity and alterations in this structure result in the development of heart dysfunction.