Mitochondrial stress requires timely intervention to prevent mitochondrial and cellular dysfunction. Re-establishing the correct protein homeostasis is crucial for coping with mitochondrial stress and maintaining cellular homeostasis. The best-characterized adaptive pathways for mitochondrial stress involve a signal originating from stressed mitochondria that triggers a nuclear response. However, recent findings have shown that mitochondrial stress also affects a complex network of protein homeostasis pathways in the cytosol. We review how mitochondrial dysregulation affects cytosolic proteostasis by regulating the quantity and quality of protein synthesis, protein stability, and protein degradation, leading to an integrated regulation of cellular metabolism and proliferation. This mitochondria to cytosol network extends the current model of the mitochondrial stress response, with potential applications in the treatment of mitochondrial disease.

线粒体应激需要及时干预，以防止线粒体和细胞功能障碍。重新建立正确的蛋白质动态平衡对于应对线粒体应激和维持细胞动态平衡至关重要。线粒体应激的最佳表征适应性途径涉及源自应激线粒体的信号，该信号触发核反应。但是，最近的发现表明，线粒体应激还影响细胞溶质中蛋白质稳态通道的复杂网络。我们审查了线粒体失调如何通过调节蛋白质合成，蛋白质稳定性和蛋白质降解的数量和质量，从而导致细胞代谢和增殖的综合调控来影响胞质蛋白稳态。