干细胞中自噬与氧化应激之间的动态相互作用:对再生医学的启示

Dynamic Interplay Between Autophagy and Oxidative Stress in Stem Cells: Implications for Regenerative Medicine.

作者信息

Rossin Daniela, Perrelli Maria-Giulia, Lo Iacono Marco, Rastaldo Raffaella, Giachino Claudia

机构信息

Department of Clinical and Biological Sciences, University of Turin, 10043 Orbassano, Italy.

出版信息

Antioxidants (Basel). 2025 Jun 6;14(6):691. doi: 10.3390/antiox14060691.

Abstract

The crosstalk between autophagy and oxidative stress is a cornerstone of stem cell biology. These processes are tightly interwoven, forming a regulatory network that impacts stem cell survival, self-renewal, and differentiation. Autophagy, a cellular recycling mechanism, ensures the removal of damaged organelles and proteins, thereby maintaining cellular integrity and metabolic balance. Oxidative stress, driven by the accumulation of reactive oxygen species (ROS), can act as both a signalling molecule and a source of cellular damage, depending on its levels and context. The interplay between autophagy and oxidative stress shapes stem cell fate by either promoting survival under stress conditions or triggering senescence and apoptosis when dysregulated. Recent evidence underscores the bidirectional relationship between these processes, where autophagy mitigates oxidative damage by degrading ROS-generating organelles, and oxidative stress can induce autophagy as a protective response. This crosstalk is critical not only for preserving stem cell function but also for addressing age-related decline and enhancing regenerative potential. Understanding the molecular mechanisms that govern this interplay offers novel insights into stem cell biology and therapeutic strategies. This review delves into the intricate molecular dynamics of autophagy and oxidative stress in stem cells, emphasizing their synergistic roles in health, disease, and regenerative medicine applications.

摘要

自噬与氧化应激之间的相互作用是干细胞生物学的基石。这些过程紧密交织,形成了一个影响干细胞存活、自我更新和分化的调控网络。自噬是一种细胞回收机制,可确保清除受损的细胞器和蛋白质,从而维持细胞完整性和代谢平衡。由活性氧(ROS)积累驱动的氧化应激,根据其水平和环境,既可以作为信号分子,也可以作为细胞损伤的来源。自噬与氧化应激之间的相互作用通过在应激条件下促进存活,或在失调时触发衰老和凋亡来塑造干细胞命运。最近的证据强调了这些过程之间的双向关系,即自噬通过降解产生活性氧的细胞器减轻氧化损伤,而氧化应激可诱导自噬作为一种保护反应。这种相互作用不仅对于维持干细胞功能至关重要,而且对于解决与年龄相关的衰退和增强再生潜力也至关重要。了解控制这种相互作用的分子机制为干细胞生物学和治疗策略提供了新的见解。本综述深入探讨了干细胞中自噬和氧化应激的复杂分子动力学,强调了它们在健康、疾病和再生医学应用中的协同作用。

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