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癌症代谢与缺血再灌注损伤:同一枚硬币的两面

Cancer Metabolism and Ischemia-Reperfusion Injury: Two Sides of the Same Coin.

作者信息

Nemeth Denise V, Baldini Enke, Sorrenti Salvatore, D'Andrea Vito, Bellini Maria Irene

机构信息

School of Osteopathic Medicine, University of the Incarnate Word, San Antonio, TX 78235, USA.

Department of Surgical Sciences, Sapienza University of Rome, 00185 Rome, Italy.

出版信息

J Clin Med. 2022 Aug 30;11(17):5096. doi: 10.3390/jcm11175096.

DOI:10.3390/jcm11175096
PMID:36079025
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9457267/
Abstract

Cancer cells are characterized by the reprogramming of certain cell metabolisms via activation of definite pathways and regulation of gene signaling. Ischemia-reperfusion injury (IRI) is characterized by tissue damage and death following a lack of perfusion and oxygenation. It is most commonly seen in the setting of organ transplantation. Interestingly, the microenvironments seen in cancer and ischemic tissues are quite similar, especially due to the hypoxic state that occurs in both. As a consequence, there is genetic signaling involved in response to IRI that has common pathways with cancer. Some of these changes are seen across the board with many cancer cells and are known as Hallmarks of Cancer, among which are aerobic glycolysis and the induction of angiogenesis. This literature review aims to compare the metabolic pathways that are altered in cancer tissues and in normal tissues subjected to IRI in order to find common adaptive processes and to identify key pathways that could represent a therapeutic target in both pathologies. By increasing our understanding of this relationship, clinical correlations can be made and applied practically to improve outcomes of transplanted organs, given the known association with acute rejection, delayed graft function, and poor graft survival. The following metabolic pathways are discussed in our review, both in the setting of cancer and IRI: apoptosis, glycolysis, and angiogenesis. The role of the immune system in both pathologies as well as mitochondrial function and the production of reactive oxygen species (ROS) are reviewed.

摘要

癌细胞的特征是通过激活特定途径和调节基因信号来对某些细胞代谢进行重编程。缺血再灌注损伤(IRI)的特征是在缺乏灌注和氧合后出现组织损伤和死亡。它最常见于器官移植的情况下。有趣的是,癌症组织和缺血组织中的微环境非常相似,特别是由于两者都存在缺氧状态。因此,对IRI的反应中涉及的基因信号与癌症有共同的途径。其中一些变化在许多癌细胞中普遍存在,被称为癌症标志,其中包括有氧糖酵解和血管生成的诱导。这篇文献综述旨在比较癌症组织和遭受IRI的正常组织中改变的代谢途径,以找到共同的适应性过程,并确定可能代表这两种病理状态治疗靶点的关键途径。鉴于已知与急性排斥、移植功能延迟和移植物存活率低有关,通过增加我们对这种关系的理解,可以建立临床相关性并实际应用于改善移植器官的结果。我们的综述讨论了以下在癌症和IRI情况下的代谢途径:细胞凋亡、糖酵解和血管生成。还综述了免疫系统在这两种病理状态中的作用以及线粒体功能和活性氧(ROS)的产生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d6a/9457267/583c08a82d97/jcm-11-05096-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d6a/9457267/3768ce918ccc/jcm-11-05096-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5d6a/9457267/3768ce918ccc/jcm-11-05096-g001.jpg
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