Caloric restriction delays yeast chronological aging by remodeling carbohydrate and lipid metabolism, altering peroxisomal and mitochondrial functionalities, and postponing the onsets of apoptotic and liponecrotic modes of regulated cell death.
Caloric restriction delays yeast chronological aging by remodeling carbohydrate and lipid metabolism, altering peroxisomal and mitochondrial functionalities, and postponing the onsets of apoptotic and liponecrotic modes of regulated cell death.
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DOI：
10.18632/oncotarget.24604
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发表时间：
2018-03-23
期刊：
影响因子：
--
通讯作者：
Titorenko VI
中科院分区：
文献类型：
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作者：
Arlia-Ciommo A;Leonov A;Beach A;Richard VR;Bourque SD;Burstein MT;Kyryakov P;Gomez-Perez A;Koupaki O;Feldman R;Titorenko VI
限制热量的饮食方案可以延缓进化距离较远的真核生物的衰老，包括芽殖酵母酿酒酵母。在这里，我们评估了热量限制如何影响按时间顺序老化的酵母在老化过程的不同阶段的形态、生化和细胞生物学特性。我们的研究结果表明，这种低热量饮食通过协调进入非增殖状态之前和进入非增殖状态之后各种细胞过程的时空动态的机制来减缓酵母的时间老化。热量限制通过调整吸收以下内容的网络来逐步建立延迟衰老的细胞模式：1）碳水化合物和脂质代谢途径； 2）内质网、脂滴、过氧化物酶体、线粒体和细胞质之间的通讯； 3）线粒体融合和裂变过程之间的平衡。在衰老过程的不同阶段，这个复杂网络的热量限制依赖性重塑1）推迟了与年龄相关的受调节细胞死亡的细胞凋亡和脂肪坏死模式的发生； 2) 通过支持细胞蛋白质稳态的维持，积极增加细胞存活的机会。由于热量限制降低了细胞死亡的风险，并积极增加了细胞在整个生命周期中存活的机会，因此这种饮食干预可以延长按时间顺序老化的酵母的寿命。
A dietary regimen of caloric restriction delays aging in evolutionarily distant eukaryotes, including the budding yeast Saccharomyces cerevisiae. Here, we assessed how caloric restriction influences morphological, biochemical and cell biological properties of chronologically aging yeast advancing through different stages of the aging process. Our findings revealed that this low-calorie diet slows yeast chronological aging by mechanisms that coordinate the spatiotemporal dynamics of various cellular processes before entry into a non-proliferative state and after such entry. Caloric restriction causes a stepwise establishment of an aging-delaying cellular pattern by tuning a network that assimilates the following: 1) pathways of carbohydrate and lipid metabolism; 2) communications between the endoplasmic reticulum, lipid droplets, peroxisomes, mitochondria and the cytosol; and 3) a balance between the processes of mitochondrial fusion and fission. Through different phases of the aging process, the caloric restriction-dependent remodeling of this intricate network 1) postpones the age-related onsets of apoptotic and liponecrotic modes of regulated cell death; and 2) actively increases the chance of cell survival by supporting the maintenance of cellular proteostasis. Because caloric restriction decreases the risk of cell death and actively increases the chance of cell survival throughout chronological lifespan, this dietary intervention extends longevity of chronologically aging yeast.