
Skin is the most voluminous organ of the body. It assumes several important physiological functions and represents also a "social interface" between an individual and other members of society. This is the main reason its age-dependent modifications are in the forefront of dermatological research and of the "anti-aging" cosmetic industry. Here we concentrate on some aspects only of skin aging, as far as the cellular and extracellular matrix components of skin are concerned. Most well studied mechanisms of skin aging can be situated at the postgenetic level, both epigenetic and post-translational mechanisms being involved. Some of these mechanisms will be reviewed as well as the capacity of fucose- and rhamnose-rich oligo- and polysaccharides (FROP and RROP) to counteract several of the mechanisms involved in skin aging.
Glycation End Products, Advanced, Keratinocytes, Free Radicals, Pancreatic Elastase, Nuclear Proteins, Oligosaccharides, Receptors, Cell Surface, Fibroblasts, Lamin Type A, Rhamnose, Extracellular Matrix, Maillard Reaction, Skin Aging, Mice, Animals, Humans, Atrophy, Protein Precursors, Peptides, Fucose
Glycation End Products, Advanced, Keratinocytes, Free Radicals, Pancreatic Elastase, Nuclear Proteins, Oligosaccharides, Receptors, Cell Surface, Fibroblasts, Lamin Type A, Rhamnose, Extracellular Matrix, Maillard Reaction, Skin Aging, Mice, Animals, Humans, Atrophy, Protein Precursors, Peptides, Fucose
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