Aging: Facts and Theories by L. Robert, T. Fulop, T. Fulop

By L. Robert, T. Fulop, T. Fulop

Getting older encouraged a lot of theories attempting to rationalize the getting older procedure universal to all residing beings. during this ebook crucial environmental and intrinsic mechanisms concerned about the getting older method and in its pathological results are reviewed. moreover theoretical and experimental facts of crucial theoretical parts in keeping with Darwinian evolution, mobile getting older, position of telephone membranes, unfastened radicals and oxidative approaches, receptor-mediated reactions, the extracellular matrix and immune services in addition to an important environmental and intrinsic mechanisms thinking about the getting older procedure and in its pathological results are mentioned. those displays of theories and similar experimental evidence provide a world review of contemporary recommendations of the biology of the getting older approach and are of crucial examining not just for experts during this box but additionally for practitioners of medical, clinical, social and experimental sciences.

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In senescent human skin, due to functional changes in fibroblasts, collagen fibers are fragmented, the fibroblasts lose contact with collagen, and the ground substance increases. This leads to the destruction of the relationship between fibroblasts and interstitial matrix breaking the relationship between the fibroblast cytoskeleton, the plasma membrane, fibronectin, and collagen [140]. The drop in glycosaminoglycan content in old age contributes to this modified relationship [141]. There is a causal relationship between changes in vascular compliance and the evolution of the collagen/elastin ratio, and the proportion of endothelial and smooth muscle cells.

5 or 3% oxygen concentration delayed the appearance of replicative senescence compared to cells grown in 20% and resulted in reduced expression levels of the cell cycle modulators p21 and p16 [22]. Late passage fibroblasts have extended replicative capacity under 3% as compared to 20% oxygen, but have significantly shorter telomere lengths [23]. These results are consistent with the idea that critically short telomere length may not be the sole trigger of cell senescence. Treatment of human fibroblasts with 5-azacytidine [24] and with 8-methoxypsoralen and subsequent ultraviolet A irradiation [25] resulted in a permanent switch to postmitotic cells.

These data raise the possibility that lamin A, which is mutated in this syndrome and is expressed in fibroblasts but not in hematopoietic cells, decreases telomere length. In benign leiomyoma tumors, telomere size is unrelated with the proliferation potential [66]. In malignant human tissues, results are variable. Nonisotropic Southern hybridization revealed a reduction of telomere repeat arrays in 14 of the 35 tumors analyzed. In other cases, 60% showed either no reduction or an increase in telomere length [67].

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