Communications biology · 2023
Lifespan-extending interventions induce consistent patterns of fatty acid oxidation in mouse livers.
СтатьяПоддержка исследования: вне правительства СШАПоддержка NIH: внешняя программаНазвание и аннотация: Перевод пока не подготовлен
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История · было → стало
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Watanabe Kengo, Wilmanski Tomasz, Baloni Priyanka, Robinson Max, Garcia Gonzalo G, Hoopmann Michael R, Midha Mukul K, Baxter David H, Maes Michal, Morrone Seamus R, Crebs Kelly M, Kapil Charu, Kusebauch Ulrike, Wiedrick Jack, Lapidus Jodi, Pflieger Lance, Lausted Christopher, Roach Jared C, Glusman Gwênlyn, Cummings Steven R, Schork Nicholas J, Price Nathan D, Hood Leroy, Miller Richard A, Moritz Robert L, Rappaport Noa
Аннотация
Aging manifests as progressive deteriorations in homeostasis, requiring systems-level perspectives to investigate the gradual molecular dysregulation of underlying biological processes. Here, we report systemic changes in the molecular regulation of biological processes under multiple lifespan-extending interventions. Differential Rank Conservation (DIRAC) analyses of mouse liver proteomics and transcriptomics data show that mechanistically distinct lifespan-extending interventions (acarbose, 17α-estradiol, rapamycin, and calorie restriction) generally tighten the regulation of biological modules. These tightening patterns are similar across the interventions, particularly in processes such as fatty acid oxidation, immune response, and stress response. Differences in DIRAC patterns between proteins and transcripts highlight specific modules which may be tightened via augmented cap-independent translation. Moreover, the systemic shifts in fatty acid metabolism are supported through integrated analysis of liver transcriptomics data with a mouse genome-scale metabolic model. Our findings highlight the power of systems-level approaches for identifying and characterizing the biological processes involved in aging and longevity.