当线粒体融合蛋白2（MFN2）遇上自噬：衰老肌肉的新时代。
When MFN2 (mitofusin 2) met autophagy: A new age for old muscles.
作者信息
Sebastián David, Zorzano Antonio
机构信息
a Institute for Research in Biomedicine (IRB Barcelona), The Barcelona Institute of Science and Technology , Barcelona , Spain.
b Departament de Bioquímica i Biomedicina Molecular , Facultat de Biologia , Universitat de Barcelona , Barcelona , Spain.
出版信息
Autophagy. 2016 Nov;12(11):2250-2251. doi: 10.1080/15548627.2016.1215383. Epub 2016 Aug 30.
A long-standing quest is to define the mechanisms responsible for the mitochondrial dysfunction and accumulation of damaged mitochondria that occur during aging. Indeed, those defects are considered major contributors to the aging process. We have analyzed the effect of aging on the muscle expression of Mfn2 and the impact of Mfn2 ablation on muscle function. Our findings reveal that Mfn2 is repressed in muscle during aging, and that is a determinant for the inhibition of autophagy, and mitochondrial quality control, which lead to the accumulation of damaged mitochondria.
长期以来的一个探索目标是确定导致衰老过程中出现的线粒体功能障碍和受损线粒体积累的机制。事实上，这些缺陷被认为是衰老过程的主要促成因素。我们分析了衰老对肌肉中Mfn2表达的影响以及Mfn2缺失对肌肉功能的影响。我们的研究结果表明，衰老过程中肌肉中的Mfn2受到抑制，这是抑制自噬和线粒体质量控制的一个决定因素，而这会导致受损线粒体的积累。
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