{"title":"Role of Apoptosis-Related Proteins P53 and Bcl-2 in the Pathogenesis of Nervous System Diseases","authors":"E. D. Bazhanova, A. A. Kozlov","doi":"10.1134/s0022093024040173","DOIUrl":null,"url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Abstract</h3><p>Diseases of the central nervous system occupy a leading place\nalong with cardiovascular and oncological diseases, and the proportion\nof patients suffering from them is increasing as the population ages.\nThis group of diseases encompasses acute conditions, such as ischemic\nstroke, and chronic multifactorial diseases, e.g., Alzheimer’s and\nParkinson’s diseases, epilepsy, etc. The development of specific\nmethods for their treatment is difficult, while the efficacy of\nthe available drugs is quite low. Almost all brain diseases are\nunderlain by common mechanisms, such as oxidative stress, inflammation, and\nneuronal death. Most often, cells die through apoptosis caused by\nan imbalance of pro- and anti-apoptotic factors. This review article\naddresses two of them, the pro-apoptotic transcription factor and tumor\nsuppressor protein p53 and its opponent, the anti-apoptotic B-cell\nlymphoma 2 (Bcl-2) protein. The choice of these proteins for special\nconsideration owes to the fact that both of them are key regulators\nof apoptosis and matter greatly in the pathogenesis of nervous diseases\nbecause neurons are not highly proliferative cells. The p53 protein\nis involved in the regulation of many genes responsible for DNA\nrepair, apoptosis, and other biochemical intracellular processes,\nwhich is particularly important when studying neuronal pathology.\nBcl-2 suppresses apoptosis in various cells, including neurons,\nby controlling mitochondrial membrane permeability and inhibiting\ncaspases. In diseases, its expression can either increase, for example,\nin the case of malignant tumors, or decrease, as in the case of neurodegenerative\nprocesses. As has been established, p53 and Bcl-2 closely interact\nwhile regulating apoptosis, and their ratio may be an important\nprognostic factor. This work was aimed to assess the role of these\nproteins in the pathogenesis of various diseases of the nervous\nsystem, and to characterize common dynamic patterns of their expression\nand coexpression.</p>","PeriodicalId":0,"journal":{"name":"","volume":null,"pages":null},"PeriodicalIF":0.0,"publicationDate":"2024-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1134/s0022093024040173","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
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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