Abstract
The mechanisms of aging and of age-dependent pathologies can be studied at the tissue level. Such studies concern cell aging within tissues, where cells are surrounded by their matrix. Matrix components undergo post-synthetic modifications such as the Maillard reaction and proteolytic degradations. Finally, cell matrix interactions, mediated by cell membrane receptors also undergo age-dependent modifications. These three aspects of tissue-aging are discussed succinctly in this review with several examples, as the age-dependent increase of fibronectin and the potential harmful effects of its degradation products and the age-dependent degradation of elastin and the harmful effects of elastin peptides mediated by the elastin-laminin receptor. These examples clearly show the intricate cooperation of gene-mediated processes (increased expression of fibronectin and some elastolytic enzymes) and of post-synthetic processes as the novel properties of fibronectin and elastin derived peptides. Such epigenetic mechanisms appear to play a crucial role in age-dependent tissue alterations and pathologies.
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