Role of Apoptosis-Related Proteins P53 and Bcl-2 in the Pathogenesis of Nervous System Diseases

Pub Date : 2024-08-29 DOI:10.1134/s0022093024040173

E. D. Bazhanova, A. A. Kozlov

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Abstract

Diseases of the central nervous system occupy a leading place along with cardiovascular and oncological diseases, and the proportion of patients suffering from them is increasing as the population ages. This group of diseases encompasses acute conditions, such as ischemic stroke, and chronic multifactorial diseases, e.g., Alzheimer’s and Parkinson’s diseases, epilepsy, etc. The development of specific methods for their treatment is difficult, while the efficacy of the available drugs is quite low. Almost all brain diseases are underlain by common mechanisms, such as oxidative stress, inflammation, and neuronal death. Most often, cells die through apoptosis caused by an imbalance of pro- and anti-apoptotic factors. This review article addresses two of them, the pro-apoptotic transcription factor and tumor suppressor protein p53 and its opponent, the anti-apoptotic B-cell lymphoma 2 (Bcl-2) protein. The choice of these proteins for special consideration owes to the fact that both of them are key regulators of apoptosis and matter greatly in the pathogenesis of nervous diseases because neurons are not highly proliferative cells. The p53 protein is involved in the regulation of many genes responsible for DNA repair, apoptosis, and other biochemical intracellular processes, which is particularly important when studying neuronal pathology. Bcl-2 suppresses apoptosis in various cells, including neurons, by controlling mitochondrial membrane permeability and inhibiting caspases. In diseases, its expression can either increase, for example, in the case of malignant tumors, or decrease, as in the case of neurodegenerative processes. As has been established, p53 and Bcl-2 closely interact while regulating apoptosis, and their ratio may be an important prognostic factor. This work was aimed to assess the role of these proteins in the pathogenesis of various diseases of the nervous system, and to characterize common dynamic patterns of their expression and coexpression.

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凋亡相关蛋白 P53 和 Bcl-2 在神经系统疾病发病机制中的作用

摘要中枢神经系统疾病与心血管疾病和肿瘤疾病并列居首位，随着人口老龄化的加剧，中枢神经系统疾病患者的比例也在不断增加。开发治疗这些疾病的特殊方法十分困难，而现有药物的疗效却很低。几乎所有脑部疾病都有共同的发病机制，如氧化应激、炎症和神经元死亡。大多数情况下，细胞是通过促凋亡因子和抗凋亡因子失衡导致的细胞凋亡而死亡的。这篇综述文章探讨了其中的两种因子，即促凋亡转录因子和肿瘤抑制蛋白 p53 及其对手--抗凋亡 B 细胞淋巴瘤 2（Bcl-2）蛋白。之所以选择这两种蛋白进行特别研究，是因为它们都是细胞凋亡的关键调节因子，在神经疾病的发病机制中起着重要作用，因为神经元不是高度增殖的细胞。p53 蛋白参与调控许多负责 DNA 修复、细胞凋亡和其他细胞内生化过程的基因，这在研究神经元病理学时尤为重要。Bcl-2 通过控制线粒体膜的通透性和抑制天冬酶来抑制包括神经元在内的各种细胞的凋亡。在疾病中，Bcl-2 的表达既可能增加（如恶性肿瘤），也可能减少（如神经退行性过程）。正如已经证实的那样，p53 和 Bcl-2 在调控细胞凋亡的同时密切相互作用，它们的比例可能是一个重要的诊断因素。这项工作旨在评估这些蛋白在神经系统各种疾病的发病机制中的作用，并描述它们表达和共表达的共同动态模式。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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