Aging, from basic research to pathological applications.
This introductory chapter tentatively draws a parallel between some of the highlights of basic aging research and their incidence for the understanding of age-associated pathologies. Some of the most important mechanisms described for cell- and tissue-aging, such as limited cell-proliferation, "parasitic" reactions, such as non-enzymatic glycation, ROS-production, uncontrolled proteolysis involving matricryptic sites, receptor loss and uncoupling appear to be the most promising links between those two approaches to fundamental and clinical gerontology. Some of the "parasitic", epigenetic, post-translational reactions lead to vicious circles which over the years might well produce cell- and tissue-damage as seen in most age-associated diseases. There is little doubt that the better understanding of these relationships will also prove helpful for pharmacological research as related to the age-associated pathologies.
Robert
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Laboratoire de Recherche Ophtalmologique, Université Paris 6, Hôpital Hôtel Dieu, 1, place du Parvis-Notre-Dame, 75181 Paris 4, France. lrobert1@compuserve.com
Robert
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D000368:Aged; D000375:Aging / Q000502:physiology*; D002455:Cell Division; D004261:DNA Replication; D006801:Humans; D010336:Pathology; D014176:Protein Biosynthesis; D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic / Q000502:physiology; D012106:Research / Q000639:trends; D014158:Transcription, Genetic
D000067759:Receptor for Advanced Glycation End Products; D011971:Receptors, Immunologic