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Biogerontology. 2002;3(6):325-35.

Aging of myocardial collagen.

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  • 1Department of Anatomy, Institute of Biomedical Sciences, University of São Paulo, Brazil. souzarrd@uol.com.br

Abstract

The objective of this article was to present a review of the collagen tissue of the heart muscle as a function of age. The myocardial collagen matrix consists of a network of fibrillar collagen which is intimately connected to the myocyte. Most collagen fibers reside in parallel with myocytes. These fibers may have a wavy, taut or coiled appearance. Fibrillar collagen types I and III are the major components of the myocardial collagen matrix. Collagen type I has been found to represent nearly 80% of the total collagen protein, while type III collagen is present in lower proportions (approximately 11%). Cardiac fibroblasts are the cellular source of fibrillar collagen, cardiac myocytes expressing only mRNA for type IV collagen. Collagens types I and III exhibit a high tensile strength which plays an important role in the behavior of the ventricle during the cardiac cycle. The collagen concentration and the intermolecular cross-linking of collagen increase with age. Measurements of collagen content in myocardial tissue suggest that it is the type I collagen fibers that increase in number and thickness in the aged. At the same time, electron microscopic observations have shown an increase in the number of collagen fibrils with a large diameter in the aging heart. The mechanism responsible for the myocardial fibrosis in the senescent myocardium is unclear. The collagen deposition in the myocardium could be due to the regulation of collagen biosynthesis at pre-translational levels. It is possible that the regulatory elements involved in this process are growth factors such as TGF-beta 1 and hormones and neurotransmitters. Details of regulatory mechanism that may come into play during aging may be elucidated by further investigations. The accumulation of collagen within the myocardium increases muscle stiffness. Myocardial function is affected by this process; this is usually reflected by incomplete relaxation during early diastolic filling, and presumably account for the decrease in early left ventricular diastolic compliance.

PMID:
12510171
[PubMed - indexed for MEDLINE]
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