R&D Center, OneCureGEN Co., Ltd, Daejeon, 34141, Republic of Korea; Department of Pathology and Laboratory Medicine, Weill Cornell Medicine, New York, NY, 10021, USA.
University of Chicago, Chicago, IL, 60637, USA.
Free Radic Biol Med. 2021 Jun;169:74-83. doi: 10.1016/j.freeradbiomed.2021.03.043. Epub 2021 Apr 18.
Neural stem/progenitor cells (NSPCs) contribute to the physiological cellular turnover of the adult brain and make up its regenerative potential. It is thus essential to understand how different factors influence their proliferation and differentiation to gain better insight into potential therapeutic targets in neurodegenerative diseases and traumatic brain injuries. Recent evidences indicate the roles of redox stress sensing and coping mechanisms in mediating the balance between NSPC self-renewal and differentiation. Such mechanisms involve direct cysteine modification, signaling and metabolic reprogramming, epigenetic alterations and transcription changes leading to adaptive responses like autophagy. Here, we discuss emerging findings on the involvement of redox sensors and effectors and their mechanisms in influencing changes in cellular redox potential and NSPC fate.
神经干细胞/祖细胞(NSPCs)为成年大脑的生理细胞更新做出贡献,并构成其再生潜力。因此,了解不同因素如何影响它们的增殖和分化对于深入了解神经退行性疾病和创伤性脑损伤的潜在治疗靶点至关重要。最近的证据表明,氧化还原应激感应和应对机制在调节 NSPC 自我更新和分化之间的平衡中发挥作用。这些机制涉及直接半胱氨酸修饰、信号转导和代谢重编程、表观遗传改变和转录变化,导致自噬等适应性反应。在这里,我们讨论了氧化还原传感器和效应器及其机制在影响细胞氧化还原电位和 NSPC 命运变化中的作用的新发现。