Mitochondria are organized in the cell in the form of a dynamic, interconnected network. Mitochondrial dynamics, regulated by mitochondrial fission, fusion, and trafficking, ensure restructuring of this complex reticulum in response to nutrient availability, molecular signals, and cellular stress. Aberrant mitochondrial structures have long been observed in aging and age-related diseases indicating that mitochondrial dynamics are compromised as cells age. However, the specific mechanisms by which aging affects mitochondrial dynamics and whether these changes are causally or casually associated with cellular and organismal aging is not clear. Here, we review recent studies that show specifically how mitochondrial fission, fusion, and trafficking are altered with age. We discuss factors that change with age to directly or indirectly influence mitochondrial dynamics while examining causal roles for altered mitochondrial dynamics in healthy aging and underlying functional outputs that might affect longevity. Lastly, we propose that altered mitochondrial dynamics might not just be a passive consequence of aging but might constitute an adaptive mechanism to mitigate age-dependent cellular impairments and might be targeted to increase longevity and promote healthy aging.

中文翻译：

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线粒体动力学在长寿和健康衰老中的因果作用。

线粒体以动态，相互连接的网络的形式组织在细胞中。线粒体的动力学受线粒体裂变，融合和运输的调节，可确保对这种复杂的网状结构进行重组，以响应养分的可利用性，分子信号和细胞应激。长期以来，在衰老和与年龄有关的疾病中观察到异常的线粒体结构，表明线粒体动力学随着细胞的衰老而受到损害。但是，尚不清楚衰老影响线粒体动力学的具体机制以及这些变化与细胞和机体衰老是因果关系还是偶然发生的。在这里，我们回顾了最近的研究，这些研究具体显示了线粒体的裂变，融合和运输如何随年龄而改变。我们讨论了随年龄变化而直接或间接影响线粒体动力学的因素，同时研究了健康衰老过程中线粒体动力学变化的因果作用以及可能影响寿命的潜在功能输出。最后，我们提出改变线粒体动力学可能不仅是衰老的被动结果，而且可能构成一种适应机制，以减轻年龄依赖性细胞损伤，并可能旨在延长寿命和促进健康衰老。