
The purpose of this paper is to review and to illustrate some of the themes underlying recent research on the aging of connective tissues. The systematic variation with age of the relative rates of biosynthesis (and of degradation) of the macromolecules of the intercellular matrix (collagens, elastin, proteoglycans and structural glycoproteins) is interpreted as the result of an "age program" of matrix synthesis by differentiated mesenchymal cells. This relative rates of synthesis of a well-defined set of matrix macromolecules can be used in its turn to define the state of differentiation (and of aging) of mesenchymal cells. This relative rate of synthesis of a well-defined set of matrix macromole-followed by its degradation through the elastases. The increasing frequency of some diseases with age ("aging diseases" of connective tissues, athero-/arteriosclerosis, diabetes, osteoarticular diseases, etc.) is probably related to this changing composition of the intercellular matrix. Cell-matrix interaction does depend on the secretion of a specific matrix which in its turn influences cell behaviour. With changing matrix composition (changing cell environment) cell behaviour will also change. This informational feedback mechanism may be of great importance in the aging of connective tissues and also in the increasing frequency of some pathologies with age.
Adult, Aging, Adolescent, Pancreatic Elastase, Arteriosclerosis, DNA, Growth, Middle Aged, Elastic Tissue, Elastin, Connective Tissue, Animals, Humans, Proteoglycans, Rabbits, Collagen, Child, Aorta, Connective Tissue Cells, Aged, Glycoproteins
Adult, Aging, Adolescent, Pancreatic Elastase, Arteriosclerosis, DNA, Growth, Middle Aged, Elastic Tissue, Elastin, Connective Tissue, Animals, Humans, Proteoglycans, Rabbits, Collagen, Child, Aorta, Connective Tissue Cells, Aged, Glycoproteins
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