Summary
Fibrillar collagen is an essential component of the extracellular matrix of the heart that surrounds and interconnects the coronary microcirculation, individual myocytes, groups of cardiac myofibrils, muscle fibers, and muscle fiber bundles. Accordingly, it provides for cardiac myocyte and muscle fiber alignment, and in so doing it imparts a mechanical support to the myocardium that assists in the maintenance of ventricular shape, size, and function. Interstitial fibrillar collagen concentration is known to be increased from 40% to 150% in genetic and experimental left-ventricular hypertension and with pathological elevations of circulating angiotensin II or mineralocorticoids. A significant portion of this fibrosis may be related to multifocal myocyte necrosis and intramyocardial coronary artery damage, which occur in these models. As a consequence of this increase in fibrillar collagen, both the myocardium and the ventricle become stiffer. Systolic function is preserved by the accompanying hypertrophy and enhanced contractility unless the increase in myocardial collagen consists of a significant degree of endomyocardial reparative fibrosis. In contrast, chronic volume overload induces an increase in myocardial collagenase activity with subsequent collagen degradation that results in ventricular dilatation and a decrease in ventricular stiffness. The ventricular dilatation, change in ventricular shape, and increase in distensibility in dilated cardiomyopathy and end-stage heart failure are also mediated by collagenase activation and fibrillar collagen breakdown.
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Janicki, J.S., Campbell, S.E., Henegar, J.R., Brower, G.L. (1997). Myocardial Interstitial Collagen Matrix Remodeling in Response to a Chronic Elevation in Ventricular Preload or Afterload. In: Maruyama, Y., Hori, M., Janicki, J.S. (eds) Cardiac-Vascular Remodeling and Functional Interaction. Springer, Tokyo. https://doi.org/10.1007/978-4-431-67041-4_3
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DOI: https://doi.org/10.1007/978-4-431-67041-4_3
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