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The Regulation of Collagen Deposition in the Hypertrophying Heart

Collagens are the major extracellular matrix proteins in the heart, contributing to diastolic stiffness, maintenance of functional capacity and determination of cell phenotype. They are continuously synthesized and degraded throughout life, a balance between these processes being critical for the continued normal function of the myocardium. The fibrillar collagens, types I and I11 are most abundant, forming the weaves and struts of the collagen network described by Borg & Caulfield.' During the development of cardiac hypertrophy collagen deposition occurs. This may result in no change in collagen concentration, reflecting a coordinate increase in the myocardial contractile component and extracellular matrix; or an increase in collagen concentration, seen in the later stages after pressure overload, leading to cardiac fibrosis. Although an increase in content in the compensatory stage of hypertrophy may be beneficial, as the matrix grows to accommodate the hypertrophied muscle, increased concentration increases diastolic stiffness, which may contribute to eventual heart failure. For this reason there is now great interest in the pathways that regulate collagen deposition.