Aneuploidy, inflammation and diseases

IF 1.5 4区 医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY Mutation Research-Fundamental and Molecular Mechanisms of Mutagenesis Pub Date : 2022-01-01 DOI:10.1016/j.mrfmmm.2022.111777
Micheline Kirsch-Volders , Michael Fenech
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引用次数: 3

Abstract

This review discusses how numerical aneuploidy may trigger inflammation in somatic cells and its consequences. Therefore we: i) summarized current knowledge on the cellular and molecular pathological effects of aneuploidy; ii) considered which of these aspects are able to trigger inflammation; iii) determined the genetic and environmental factors which may modulate the link between aneuploidy and inflammation; iv) explored the rôle of diet in prevention of aneuploidy and inflammation; v) examined whether aneuploidy and inflammation are causes and/or consequences of diseases; vi) identified the knowledge gaps and research needed to translate these observations into improved health care and disease prevention.

The relationships between aneuploidy, inflammation and diseases are complex, because they depend on which chromosomes are involved, the proportion of cells affected and which organs are aneuploid in the case of mosaic aneuploidy. Therefore, a systemic approach is recommended to understand the emergence of aneuploidy-driven diseases and to take preventive measures to protect individuals from exposure to aneugenic conditions.

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非整倍体,炎症和疾病
本文综述了数值非整倍体如何引发体细胞炎症及其后果。因此,我们:i)总结了目前关于非整倍体的细胞和分子病理效应的知识;Ii)考虑这些方面中哪一个能够引发炎症;Iii)确定可能调节非整倍体与炎症之间联系的遗传和环境因素;Iv)探讨饮食在预防非整倍体和炎症中的rôle作用;V)检查非整倍体和炎症是否是疾病的原因和/或后果;(六)确定了将这些观察结果转化为改善保健和疾病预防所需的知识差距和研究。非整倍体、炎症和疾病之间的关系是复杂的,因为它们取决于涉及哪些染色体、受影响的细胞比例以及在马赛克非整倍体的情况下哪些器官是非整倍体。因此,建议采用系统的方法来了解非整倍体驱动疾病的出现,并采取预防措施来保护个体免受非优生条件的影响。
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来源期刊
CiteScore
4.90
自引率
0.00%
发文量
24
审稿时长
51 days
期刊介绍: Mutation Research (MR) provides a platform for publishing all aspects of DNA mutations and epimutations, from basic evolutionary aspects to translational applications in genetic and epigenetic diagnostics and therapy. Mutations are defined as all possible alterations in DNA sequence and sequence organization, from point mutations to genome structural variation, chromosomal aberrations and aneuploidy. Epimutations are defined as alterations in the epigenome, i.e., changes in DNA methylation, histone modification and small regulatory RNAs. MR publishes articles in the following areas: Of special interest are basic mechanisms through which DNA damage and mutations impact development and differentiation, stem cell biology and cell fate in general, including various forms of cell death and cellular senescence. The study of genome instability in human molecular epidemiology and in relation to complex phenotypes, such as human disease, is considered a growing area of importance. Mechanisms of (epi)mutation induction, for example, during DNA repair, replication or recombination; novel methods of (epi)mutation detection, with a focus on ultra-high-throughput sequencing. Landscape of somatic mutations and epimutations in cancer and aging. Role of de novo mutations in human disease and aging; mutations in population genomics. Interactions between mutations and epimutations. The role of epimutations in chromatin structure and function. Mitochondrial DNA mutations and their consequences in terms of human disease and aging. Novel ways to generate mutations and epimutations in cell lines and animal models.
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