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Dietary Restriction and AMPK Increase Lifespan via Mitochondrial Network and Peroxisome Remodeling.
Cell Metabolism ( IF 27.7 ) Pub Date : 2017-Dec-05 , DOI: 10.1016/j.cmet.2017.09.024 Heather J Weir 1 , Pallas Yao 1 , Frank K Huynh 2 , Caroline C Escoubas 1 , Renata L Goncalves 1 , Kristopher Burkewitz 1 , Raymond Laboy 1 , Matthew D Hirschey 2 , William B Mair 1
Cell Metabolism ( IF 27.7 ) Pub Date : 2017-Dec-05 , DOI: 10.1016/j.cmet.2017.09.024 Heather J Weir 1 , Pallas Yao 1 , Frank K Huynh 2 , Caroline C Escoubas 1 , Renata L Goncalves 1 , Kristopher Burkewitz 1 , Raymond Laboy 1 , Matthew D Hirschey 2 , William B Mair 1
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Mitochondrial network remodeling between fused and fragmented states facilitates mitophagy, interaction with other organelles, and metabolic flexibility. Aging is associated with a loss of mitochondrial network homeostasis, but cellular processes causally linking these changes to organismal senescence remain unclear. Here, we show that AMP-activated protein kinase (AMPK) and dietary restriction (DR) promote longevity in C. elegans via maintaining mitochondrial network homeostasis and functional coordination with peroxisomes to increase fatty acid oxidation (FAO). Inhibiting fusion or fission specifically blocks AMPK- and DR-mediated longevity. Strikingly, however, preserving mitochondrial network homeostasis during aging by co-inhibition of fusion and fission is sufficient itself to increase lifespan, while dynamic network remodeling is required for intermittent fasting-mediated longevity. Finally, we show that increasing lifespan via maintaining mitochondrial network homeostasis requires FAO and peroxisomal function. Together, these data demonstrate that mechanisms that promote mitochondrial homeostasis and plasticity can be targeted to promote healthy aging.
中文翻译：
饮食限制和 AMPK 通过线粒体网络和过氧化物酶体重塑延长寿命。
融合状态和碎片状态之间的线粒体网络重塑有利于线粒体自噬、与其他细胞器的相互作用以及代谢灵活性。衰老与线粒体网络稳态的丧失有关，但将这些变化与机体衰老联系起来的细胞过程仍不清楚。在这里，我们发现 AMP 激活蛋白激酶 (AMPK) 和饮食限制 (DR) 通过维持线粒体网络稳态和与过氧化物酶体的功能协调来增加脂肪酸氧化 (FAO)，从而促进线虫的寿命。抑制融合或裂变可特异性阻断 AMPK 和 DR 介导的寿命。然而，引人注目的是，通过共同抑制融合和裂变来维持衰老过程中线粒体网络的稳态本身就足以延长寿命，而动态网络重塑是间歇性禁食介导的长寿所必需的。最后，我们表明，通过维持线粒体网络稳态来延长寿命需要FAO和过氧化物酶体功能。总之，这些数据表明促进线粒体稳态和可塑性的机制可以有针对性地促进健康衰老。
更新日期：2017-10-27
中文翻译：
饮食限制和 AMPK 通过线粒体网络和过氧化物酶体重塑延长寿命。
融合状态和碎片状态之间的线粒体网络重塑有利于线粒体自噬、与其他细胞器的相互作用以及代谢灵活性。衰老与线粒体网络稳态的丧失有关，但将这些变化与机体衰老联系起来的细胞过程仍不清楚。在这里，我们发现 AMP 激活蛋白激酶 (AMPK) 和饮食限制 (DR) 通过维持线粒体网络稳态和与过氧化物酶体的功能协调来增加脂肪酸氧化 (FAO)，从而促进线虫的寿命。抑制融合或裂变可特异性阻断 AMPK 和 DR 介导的寿命。然而，引人注目的是，通过共同抑制融合和裂变来维持衰老过程中线粒体网络的稳态本身就足以延长寿命，而动态网络重塑是间歇性禁食介导的长寿所必需的。最后，我们表明，通过维持线粒体网络稳态来延长寿命需要FAO和过氧化物酶体功能。总之，这些数据表明促进线粒体稳态和可塑性的机制可以有针对性地促进健康衰老。
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