Mitochondria entail an incredible dynamism in their morphology, impacting death signaling and selective elimination of the damaged organelles. In turn, by recycling the superfluous or malfunctioning mitochondria, mostly prevalent during aging, mitophagy contributes to maintain a healthy mitochondrial network. Mitofusins locate at the outer mitochondrial membrane and control the plastic behavior of mitochondria, by mediating fusion events. Besides deciding on mitochondrial interconnectivity, mitofusin 2 regulates physical contacts between mitochondria and the endoplasmic reticulum, but also serves as a decisive docking platform for mitophagy and apoptosis effectors. Thus, mitofusins integrate multiple bidirectional inputs from and into mitochondria and ensure proper energetic and metabolic cellular performance. Here, we review the role of mitofusins and mitophagy at the cross-road between life and apoptotic death decisions. Furthermore, we highlight the impact of this interplay on disease, focusing on how mitofusin 2 and mitophagy affect non-alcoholic fatty liver disease.

线粒体的形态具有令人难以置信的活力，影响死亡信号并选择性消除受损的细胞器。反过来，线粒体通过回收多余的或功能异常的线粒体（在衰老过程中普遍存在），有助于维持健康的线粒体网络。线粒体融合蛋白位于线粒体外膜，并通过介导融合事件控制线粒体的塑性行为。除了决定线粒体的互连性之外，线粒体融合蛋白2还调节线粒体和内质网之间的物理接触，但它也是线粒体和细胞凋亡效应子的决定性对接平台。因此，线粒体融合素整合了来自线粒体的多个双向输入，并确保适当的能量和代谢细胞性能。这里，我们回顾了丝裂霉素和线粒体在生命与凋亡死亡决策之间的交叉作用。此外，我们重点研究了这种相互作用对疾病的影响，重点是线粒体融合蛋白2和线粒体如何影响非酒精性脂肪肝疾病。