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Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts
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| Zeitschriftentitel: | Annual Review of Physiology |
|---|---|
| Personen und Körperschaften: | , |
| In: | Annual Review of Physiology, 75, 2013, 1, S. 621-644 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
Annual Reviews
|
| Schlagwörter: |
| author_facet |
Gems, David Partridge, Linda Gems, David Partridge, Linda |
|---|---|
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Gems, David Partridge, Linda |
| spellingShingle |
Gems, David Partridge, Linda Annual Review of Physiology Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts Physiology |
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gems, david |
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Gems, David Partridge, Linda 0066-4278 1545-1585 Annual Reviews Physiology http://dx.doi.org/10.1146/annurev-physiol-030212-183712 <jats:p> Discovering the biological basis of aging is one of the greatest remaining challenges for science. Work on the biology of aging has discovered a range of interventions and pathways that control aging rate. A picture is emerging of a signaling network that is sensitive to nutritional status and that controls growth, stress resistance, and aging. This network includes the insulin/IGF-1 and target of rapamycin (TOR) pathways and likely mediates the effects of dietary restriction on aging. Yet the biological processes upon which these pathways act to control life span remain unclear. A long-standing guiding assumption about aging is that it is caused by wear and tear, particularly damage at the molecular level. One view is that reactive oxygen species (ROS), including free radicals, generated as by-products of cellular metabolism, are a major contributor to this damage. Yet many recent tests of the oxidative damage theory have come up negative. Such tests have opened an exciting new phase in biogerontology in which fundamental assumptions about aging are being reexamined and revolutionary concepts are emerging. Among these concepts is the hyperfunction theory, which postulates that processes contributing to growth and reproduction run on in later life, leading to hypertrophic and hyperplastic pathologies. Here we reexamine central concepts about the nature of aging. </jats:p> Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts Annual Review of Physiology |
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| title |
Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
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Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
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Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
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Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
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Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
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Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
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genetics of longevity in model organisms: debates and paradigm shifts |
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Physiology |
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http://dx.doi.org/10.1146/annurev-physiol-030212-183712 |
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2013 |
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621-644 |
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<jats:p> Discovering the biological basis of aging is one of the greatest remaining challenges for science. Work on the biology of aging has discovered a range of interventions and pathways that control aging rate. A picture is emerging of a signaling network that is sensitive to nutritional status and that controls growth, stress resistance, and aging. This network includes the insulin/IGF-1 and target of rapamycin (TOR) pathways and likely mediates the effects of dietary restriction on aging. Yet the biological processes upon which these pathways act to control life span remain unclear. A long-standing guiding assumption about aging is that it is caused by wear and tear, particularly damage at the molecular level. One view is that reactive oxygen species (ROS), including free radicals, generated as by-products of cellular metabolism, are a major contributor to this damage. Yet many recent tests of the oxidative damage theory have come up negative. Such tests have opened an exciting new phase in biogerontology in which fundamental assumptions about aging are being reexamined and revolutionary concepts are emerging. Among these concepts is the hyperfunction theory, which postulates that processes contributing to growth and reproduction run on in later life, leading to hypertrophic and hyperplastic pathologies. Here we reexamine central concepts about the nature of aging. </jats:p> |
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| description | <jats:p> Discovering the biological basis of aging is one of the greatest remaining challenges for science. Work on the biology of aging has discovered a range of interventions and pathways that control aging rate. A picture is emerging of a signaling network that is sensitive to nutritional status and that controls growth, stress resistance, and aging. This network includes the insulin/IGF-1 and target of rapamycin (TOR) pathways and likely mediates the effects of dietary restriction on aging. Yet the biological processes upon which these pathways act to control life span remain unclear. A long-standing guiding assumption about aging is that it is caused by wear and tear, particularly damage at the molecular level. One view is that reactive oxygen species (ROS), including free radicals, generated as by-products of cellular metabolism, are a major contributor to this damage. Yet many recent tests of the oxidative damage theory have come up negative. Such tests have opened an exciting new phase in biogerontology in which fundamental assumptions about aging are being reexamined and revolutionary concepts are emerging. Among these concepts is the hyperfunction theory, which postulates that processes contributing to growth and reproduction run on in later life, leading to hypertrophic and hyperplastic pathologies. Here we reexamine central concepts about the nature of aging. </jats:p> |
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| spelling | Gems, David Partridge, Linda 0066-4278 1545-1585 Annual Reviews Physiology http://dx.doi.org/10.1146/annurev-physiol-030212-183712 <jats:p> Discovering the biological basis of aging is one of the greatest remaining challenges for science. Work on the biology of aging has discovered a range of interventions and pathways that control aging rate. A picture is emerging of a signaling network that is sensitive to nutritional status and that controls growth, stress resistance, and aging. This network includes the insulin/IGF-1 and target of rapamycin (TOR) pathways and likely mediates the effects of dietary restriction on aging. Yet the biological processes upon which these pathways act to control life span remain unclear. A long-standing guiding assumption about aging is that it is caused by wear and tear, particularly damage at the molecular level. One view is that reactive oxygen species (ROS), including free radicals, generated as by-products of cellular metabolism, are a major contributor to this damage. Yet many recent tests of the oxidative damage theory have come up negative. Such tests have opened an exciting new phase in biogerontology in which fundamental assumptions about aging are being reexamined and revolutionary concepts are emerging. Among these concepts is the hyperfunction theory, which postulates that processes contributing to growth and reproduction run on in later life, leading to hypertrophic and hyperplastic pathologies. Here we reexamine central concepts about the nature of aging. </jats:p> Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts Annual Review of Physiology |
| spellingShingle | Gems, David, Partridge, Linda, Annual Review of Physiology, Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts, Physiology |
| title | Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
| title_full | Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
| title_fullStr | Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
| title_full_unstemmed | Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
| title_short | Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
| title_sort | genetics of longevity in model organisms: debates and paradigm shifts |
| title_unstemmed | Genetics of Longevity in Model Organisms: Debates and Paradigm Shifts |
| topic | Physiology |
| url | http://dx.doi.org/10.1146/annurev-physiol-030212-183712 |