Ma, S., et al. (2020). "Caloric Restriction Reprograms the Single-Cell Transcriptional Landscape of Rattus Norvegicus Aging." Cell 180(5): 984-1001 e1022.
Aging causes a functional decline in tissues throughout the body that may be delayed by caloric restriction (CR). However, the cellular profiles and signatures of aging, as well as those ameliorated by CR, remain unclear. Here, we built comprehensive single-cell and single-nucleus transcriptomic atlases across various rat tissues undergoing aging and CR. CR attenuated aging-related changes in cell type composition, gene expression, and core transcriptional regulatory networks. Immune cells were increased during aging, and CR favorably reversed the aging-disturbed immune ecosystem. Computational prediction revealed that the abnormal cell-cell communication patterns observed during aging, including the excessive proinflammatory ligand-receptor interplay, were reversed by CR. Our work provides multi-tissue single-cell transcriptional landscapes associated with aging and CR in a mammal, enhances our understanding of the robustness of CR as a geroprotective intervention, and uncovers how metabolic intervention can act upon the immune system to modify the process of aging.
衰老会导致全身组织的功能衰退，这种衰退可能会通过限制热量摄入(CR)而延缓。然而，衰老的细胞特征和特征，以及CR改善的细胞特征，仍然不清楚。在这里，我们在衰老和CR的不同大鼠组织中构建了全面的单细胞和单核转录组图谱。CR减弱了细胞类型组成、基因表达和核心转录调控网络中与衰老相关的变化。在衰老过程中，免疫细胞增加，CR有利于逆转衰老紊乱的免疫生态系统。计算预测显示,期间观察到的异常信息交流模式老化,包括过度的促炎中的相互作用,被CR逆转。我们的工作提供了multi-tissue单细胞转录景观与哺乳动物衰老和CR,提高我们理解CR作为geroprotective干预的鲁棒性,并揭示如何代谢干预行动免疫系统可以修改老化的过程。
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