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The rules of aging: are they universal? Is the yeast model relevant for gerontology?

100%
Bilinski T., Zadrag-Tecza R.
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2014
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vol. 61
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issue 4
663-669
EN
The success of experimental biology was possible due to the use of model organisms. It is believed that the mechanisms of aging have a universal character and they are conserved in a wide range of organisms. The explanation of these universal mechanisms by tracing survival curves of model organisms clearly suggests that death of individuals is a direct consequence of aging. Furthermore, the use of unicellular organisms like yeast Saccharomyces cerevisiae to explain the aging processes of multicellular organisms runs the risk of oversimplification. Aging is a very complex process and therefore in this paper we present arguments suggesting that some of these fundamental assumptions require a deep rethinking and verification.
2
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The links between hypertrophy, reproductive potential and longevity in the Saccharomyces cerevisiae yeast

100%
Molon M., Zadrag-Tecza R.
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EN
The yeast Saccharomyces cerevisiae has long been used as a model organism for studying the basic mechanisms of aging. However, the main problem with the use of this unicellular fungus is the unit of "longevity". For all organisms, lifespan is expressed in units of time, while in the case of yeast it is defined by the number of daughter cells produced. Additionally, in yeast the phenotypic effects of mutations often show a clear dependence on the genetic background, suggesting the need for an analysis of strains representing different genetic backgrounds. Our results confirm the data presented in earlier papers that the reproductive potential is strongly associated with an increase in cell volume per generation. An excessive cell volume results in the loss of reproductive capacity. These data clearly support the hypertrophy hypothesis. The time of life of all analysed mutants, with the exception of sch9D, is the same as in the case of the wild-type strain. Interestingly, the 121% increase of the fob1D mutant's reproductive potential compared to the sfp1D mutant does not result in prolongation of the mutant's time of life (total lifespan).
3
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Calculation of the longevity of elastomeric structural elements

88%
Kozub Y., Kozub G.
Teka Commission of Motorization and Power Industry in Agriculture
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2016
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vol. 16
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issue 2
4
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Prohibitins and Ras2 protein cooperate in the maintenance of mitochondrial function during yeast aging.

88%
Kirchman P. A., Miceli M. V., West R. L., Jiang J. C., Kim S., Michal Jazwinski S.
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2003
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vol. 50
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issue 4
1039-1056
EN
The yeast Saccharomyces cerevisiae has a finite replicative life span. Yeasts possess two prohibitins, Phb1p and Phb2p, in similarity to mammalian cells. These proteins are located in the inner mitochondrial membrane, where they are involved in the processing of newly-synthesized membrane proteins. We demonstrate that the elimination of one or both of the prohibitin genes in yeast markedly diminished the replicative life span of cells that lack fully-functional mitochondria, while having no effect on cells with functioning mitochondria. This deleterious effect was suppressed by the deletion of the RAS2 gene. The expression of PHB1 and PHB2 declined gradually up to 5-fold during the life span. Cells in which PHB1 was deleted in conjunction with the absence of a mitochondrial genome displayed remarkable changes in mitochondrial morphology, distribution, and inheritance. This loss of mitochondrial integrity was not seen in cells devoid of PHB1 but possessing an intact mitochondrial genome. In a subset of the cells, the changes in mitochondrial integrity were associated with increased production of reactive oxygen species, which co-localized with the altered mitochondria. The mitochondrial deficits described above were all suppressed by deletion of RAS2. Our data, together with published information, are interpreted to provide a unified view of the role of the prohibitins in yeast aging. This model posits that the key initiating event is a decline in mitochondrial function, which leads to progressive oxidative damage that is exacerbated in the absence of the prohibitins. This aggravation of the initial damage is ameliorated by the suppression of the production of mitochondrial proteins in the absence of Ras2p signaling of mitochondrial biogenesis.
5
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Slowing down aging from within: mechanistic aspects of anti-aging hormetic effects of mild heat stress on human cells.

75%
Rattan S. I. S., Gonzalez-Dosal R., Nielsen E. R., Kraft D. C., Weibel J., Kahns S.
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vol. 51
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issue 2
481-492
EN
Since aging is primarily the result of a failure of maintenance and repair mechanisms, various approaches are being developed in order to stimulate these pathways and modulate the process of aging. One such approach, termed hormesis, involves challenging cells and organisms by mild stress that often results in anti-aging and life prolonging effects. In a series of experimental studies, we have reported that repeated mild heat stress (RMHS) has anti-aging hormetic effects on growth and various cellular and biochemical characteristics of human skin fibroblasts undergoing aging in vitro. These beneficial effects of repeated challenge include the maintenance of stress protein profile, reduction in the accumulation of oxidatively and glycoxidatively damaged proteins, stimulation of the proteasomal activities for the degradation of abnormal proteins, improved cellular resistance to other stresses, and enhanced levels of cellular antioxidant ability. In order to elucidate the molecular mechanisms of hormetic effects of RMHS, we are now undertaking studies on signal transduction pathways, energy production and utilisation kinetics, and the proteomic analysis of patterns of proteins synthesised and their posttranslational modifications in various types of human cells undergoing cellular aging in vitro. Human applications of hormesis include early intervention and modulation of the aging process to prevent or delay the onset of age-related conditions, such as sarcopenia, Alzheimer's disease, Parkinson's disease, cataracts and osteoporosis.
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