Mol. Cells 2008; 26(5): 427-435
Published online January 1, 1970
© The Korean Society for Molecular and Cellular Biology
In this review, we discuss the genes and the related signal pathways that regulate aging and longevity by reviewing recent findings of genetic longevity models in rodents in reference to findings with lower organisms. We also paid special attention to the genes and signals mediating the effects of calorie restriction (CR), a powerful intervention that slows the aging process and extends the lifespan in a range of organisms. An evolutionary view emphasizes the roles of nutrient-sensing and neuroendocrine adaptation to food shortage as the mechanisms underlying the effects of CR. Genetic and non-genetic interventions without CR suggest a role for single or combined hormonal signals that partly mediate the effect of CR. Longevity genes fall into two categories, genes relevant to nutrient-sensing systems and those associated with mitochondrial function or redox regulation. In mammals, disrupted or reduced growth hormone (GH)-insulin-like growth factor (IGF)-1 signaling robustly favors longevity. CR also suppresses the GH-IGF-1 axis, indicating the importance of this signal pathway. Surprisingly, there are very few longevity models to evaluate the enhanced anti-oxidative mechanism, while there is substantial evidence supporting the oxidative stress and damage theory of aging. Either increased or reduced mitochondrial function may extend the lifespan. The role of redox regulation and mitochondrial function in CR remains to be elucidated.
Keywords calorie restriction, longevity gene, mitochondria, neuroendocrine, nutrients
Mol. Cells 2008; 26(5): 427-435
Published online November 30, 2008
Copyright © The Korean Society for Molecular and Cellular Biology.
Isao Shimokawa, Takuya Chiba, Haruyoshi Yamaza and Toshimitsu Komatsu
In this review, we discuss the genes and the related signal pathways that regulate aging and longevity by reviewing recent findings of genetic longevity models in rodents in reference to findings with lower organisms. We also paid special attention to the genes and signals mediating the effects of calorie restriction (CR), a powerful intervention that slows the aging process and extends the lifespan in a range of organisms. An evolutionary view emphasizes the roles of nutrient-sensing and neuroendocrine adaptation to food shortage as the mechanisms underlying the effects of CR. Genetic and non-genetic interventions without CR suggest a role for single or combined hormonal signals that partly mediate the effect of CR. Longevity genes fall into two categories, genes relevant to nutrient-sensing systems and those associated with mitochondrial function or redox regulation. In mammals, disrupted or reduced growth hormone (GH)-insulin-like growth factor (IGF)-1 signaling robustly favors longevity. CR also suppresses the GH-IGF-1 axis, indicating the importance of this signal pathway. Surprisingly, there are very few longevity models to evaluate the enhanced anti-oxidative mechanism, while there is substantial evidence supporting the oxidative stress and damage theory of aging. Either increased or reduced mitochondrial function may extend the lifespan. The role of redox regulation and mitochondrial function in CR remains to be elucidated.
Keywords: calorie restriction, longevity gene, mitochondria, neuroendocrine, nutrients
Yae-Lim Lee and Cheol-Koo Lee
Mol. Cells 2008; 26(3): 299-307 https://doi.org/10.14348/.2008.26.3.299Jong Min Choi, Yongwei Piao, Kyong Hoon Ahn, Seok Kyun Kim, Jong Hoon Won, Jae Hong Lee, Ji Min Jang, In Chul Shin, Zhicheng Fu, Sung Yun Jung, Eui Man Jeong, and Dae Kyong Kim
Mol. Cells 2023; 46(9): 545-557 https://doi.org/10.14348/molcells.2023.0074Jeong-Woo Park, Jihyeon Jeong, and Young-Seuk Bae
Mol. Cells 2022; 45(3): 112-121 https://doi.org/10.14348/molcells.2021.0183