Dutysheva E A, Kuznetcova L S, Utepova I A, Margulis B A, Guzhova I V, Lazarev V F
Institute of Cytology RAS, St. Petersburg, 194064 Russian Federation.
Ural Federal University named after the first President of Russia B. N. Yeltsin, Yekaterinburg, 620002 Russian Federation.
Acta Naturae. 2025 Jan-Mar;17(1):29-35. doi: 10.32607/actanaturae.27531.
Oxidative stress accompanies many pathologies that are characterized by neuronal degradation leading to a deterioration of the disease. The main causes are the disruption of protein homeostasis and activation of irreversible processes of cell cycle disruption and deterioration of cellular physiology, leading to senescence. In this paper, we propose a new approach to combating senescence caused by oxidative stress. This approach is based on the use of a low-molecular inducer of chaperone synthesis, one of the cell protective systems regulating proteostasis and apoptosis. We present data demonstrating the ability of the pyrrolylazine derivative PQ-29 to induce chaperone accumulation in human neuronal cells and prevent oxidative stress-induced aging.
氧化应激伴随着许多以神经元退化导致疾病恶化为特征的病理状况。主要原因是蛋白质稳态的破坏以及细胞周期破坏和细胞生理恶化等不可逆过程的激活,从而导致衰老。在本文中,我们提出了一种对抗由氧化应激引起的衰老的新方法。该方法基于使用一种小分子伴侣合成诱导剂,它是调节蛋白质稳态和细胞凋亡的细胞保护系统之一。我们展示的数据表明吡咯嗪衍生物PQ - 29能够在人神经元细胞中诱导伴侣蛋白积累,并预防氧化应激诱导的衰老。