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困于返祖吸引子网络中的生命:如何寻求救援。

Life Entrapped in a Network of Atavistic Attractors: How to Find a Rescue.

作者信息

Kasperski Andrzej

机构信息

Institute of Biological Sciences, Department of Biotechnology, Laboratory of Bioinformatics and Control of Bioprocesses, University of Zielona Góra, ul. Szafrana 1, 65-516 Zielona Góra, Poland.

出版信息

Int J Mol Sci. 2022 Apr 5;23(7):4017. doi: 10.3390/ijms23074017.

DOI:10.3390/ijms23074017
PMID:35409376
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8999494/
Abstract

In view of unified cell bioenergetics, cell bioenergetic problems related to cell overenergization can cause excessive disturbances in current cell fate and, as a result, lead to a change of cell-fate. At the onset of the problem, cell overenergization of multicellular organisms (especially overenergization of mitochondria) is solved inter alia by activation and then stimulation of the reversible Crabtree effect by cells. Unfortunately, this apparently good solution can also lead to a much bigger problem when, despite the activation of the Crabtree effect, cell overenergization persists for a long time. In such a case, cancer transformation, along with the Warburg effect, may occur to further reduce or stop the charging of mitochondria by high-energy molecules. Understanding the phenomena of cancer transformation and cancer development has become a real challenge for humanity. To date, many models have been developed to understand cancer-related mechanisms. Nowadays, combining all these models into one coherent universal model of cancer transformation and development can be considered a new challenge. In this light, the aim of this article is to present such a potentially universal model supported by a proposed new model of cellular functionality evolution. The methods of fighting cancer resulting from unified cell bioenergetics and the two presented models are also considered.

摘要

鉴于细胞生物能量学的统一性,与细胞能量过剩相关的细胞生物能量问题会对当前的细胞命运造成过度干扰,进而导致细胞命运的改变。在问题出现之初,多细胞生物的细胞能量过剩(尤其是线粒体的能量过剩)可通过细胞激活并随后刺激可逆的克氏效应来解决。不幸的是,当尽管克氏效应被激活,但细胞能量过剩仍长期持续时,这个看似不错的解决方案也可能导致一个更大的问题。在这种情况下,癌症转化以及瓦氏效应可能会发生,以进一步减少或停止高能分子对线粒体的供能。理解癌症转化和癌症发展的现象已成为人类面临的一项现实挑战。迄今为止,已经开发了许多模型来理解癌症相关机制。如今,将所有这些模型整合为一个连贯的癌症转化与发展通用模型可被视为一项新挑战。有鉴于此,本文的目的是提出这样一个潜在的通用模型,并由一个提出的细胞功能进化新模型提供支持。本文还探讨了由统一细胞生物能量学及所提出的两个模型所衍生出的抗癌方法。

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