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DNA Damage and Repair in Health and Diseases
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DNA Damage and Repair in Health and Diseases

A special issue of Current Issues in Molecular Biology (ISSN 1467-3045). This special issue belongs to the section "Biochemistry, Molecular and Cellular Biology".

Deadline for manuscript submissions: 30 September 2025 | Viewed by 4283

Special Issue Editor

Prof. Dr. Tomasz Popławski

E-Mail Website
Guest Editor
Department of Pharmaceutical Microbiology and Biochemistry, Medical University of Lodz, 92-215 Lodz, Poland
Interests: DNA; epigenetics; genetic analysis; cyto- and genotoxicity; biochemistry; enzymes; metabolism
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

In human cells, DNA lesions are formed as a result of normal cell metabolic activity and various environmental factors. These represent highly serious challenges for any cell due to the tremendous number of these incidents estimated at tens of thousands per day. Many of these lesions cause structural damage to the DNA molecule, thereby altering or eliminating the cell's ability to use DNA as a source of information; therefore, DNA repair is constantly activated in response to DNA damage. At the cellular level, DNA lesions that are not repaired correctly can lead to genome instability, apoptosis and senescence, thereby significantly affecting the development and increasing the aging process of organisms. Moreover, loss of genome integrity predisposes organisms to immune deficiencies and cancer. Therefore, it is critical that cells efficiently respond to DNA damage. DNA damage response (DDR) includes not only DNA repair, but also changes in chromatin folding, signalling of DNA lesions, coordination of their repair through checkpoints, and cell death via apoptosis or senescence. In addition, transcriptome changes and energy depletion are observed in cells with damaged DNA. DNA repair capacity is critical for the integrity of normal human function. As such, this Special Issue welcomes new research papers and timely reviews on various aspects of DNA damage response in human health and diseases.

Prof. Dr. Tomasz Popławski
Guest Editor

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Keywords

  • DNA damage
  • DNA repair
  • DNA repair enzymes
  • genome stability
  • oxidative damage
  • cancers
  • autoimmune diseases

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Published Papers (3 papers)

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Research

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18 pages, 4961 KiB  
Article
Krüppel-like Factor 4-Deficient Cells Are Sensitive to Etoposide-Induced DNA Damage
by Maxwell H. Rubinstein, Aidan Conroy, Elisabeth L. Pezzuto, Hadeel Al Qoronz, Patrick Wertimer and Engda G. Hagos
Curr. Issues Mol. Biol. 2025, 47(4), 217; https://doi.org/10.3390/cimb47040217 - 21 Mar 2025
Viewed by 574
Abstract
Krüppel-like factor 4 (KLF4) is a highly conserved zinc-finger transcription factor involved in cellular processes such as development, differentiation, and cell cycle regulation. Previous studies show that mouse embryonic fibroblasts (MEFs) null for Klf4 exhibit increased genomic instability. While KLF4 is regarded as [...] Read more.
Krüppel-like factor 4 (KLF4) is a highly conserved zinc-finger transcription factor involved in cellular processes such as development, differentiation, and cell cycle regulation. Previous studies show that mouse embryonic fibroblasts (MEFs) null for Klf4 exhibit increased genomic instability. While KLF4 is regarded as a tumor suppressor in many human cancers, its role in DNA repair mechanisms remains unknown. In this study, cultured MEFs wild type (+/+) and null (−/−) for Klf4 and human carcinoma colorectal (RKO) cells were studied as a model for human colorectal cancer. Etoposide, a chemotherapeutic topoisomerase II poison, was employed to investigate KLF4’s role in DNA damage repair. Following etoposide treatment, immunostaining and Western blotting revealed cells expressing Klf4 exhibited lower levels of γ-H2AX, a biomarker for DNA damage, compared to cells without Klf4. Moreover, after DNA damage, cells expressing Klf4 exhibited increased levels of BRCA1 and Rad51, known tumor suppressor genes. Finally, genes involved in DNA damage response (DDR), ATR, and Chk1 were upregulated in cells containing functional KLF4, offering a possible mechanism for KLF4’s role in mediating DDR. Our results indicate that KLF4 plays a crucial role in maintaining genetic stability by enhancing cell DDR, supporting previous findings that KLF4 functions as a tumor suppressor. Full article
(This article belongs to the Special Issue DNA Damage and Repair in Health and Diseases)
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14 pages, 3918 KiB  
Article
Structural and Dynamic Features of the Recognition of 8-oxoguanosine Paired with an 8-oxoG-clamp by Human 8-oxoguanine-DNA Glycosylase
by Maria V. Lukina, Polina V. Zhdanova and Vladimir V. Koval
Curr. Issues Mol. Biol. 2024, 46(5), 4119-4132; https://doi.org/10.3390/cimb46050253 - 29 Apr 2024
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Abstract
8-oxoguanine (oxoG) is formed in DNA by the action of reactive oxygen species. As a highly mutagenic and the most common oxidative DNA lesion, it is an important marker of oxidative stress. Human 8-oxoguanine-DNA glycosylase (OGG1) is responsible for its prompt removal in [...] Read more.
8-oxoguanine (oxoG) is formed in DNA by the action of reactive oxygen species. As a highly mutagenic and the most common oxidative DNA lesion, it is an important marker of oxidative stress. Human 8-oxoguanine-DNA glycosylase (OGG1) is responsible for its prompt removal in human cells. OGG1 is a bifunctional DNA glycosylase with N-glycosylase and AP lyase activities. Aspects of the detailed mechanism underlying the recognition of 8-oxoguanine among numerous intact bases and its subsequent interaction with the enzyme’s active site amino acid residues are still debated. The main objective of our work was to determine the effect (structural and thermodynamic) of introducing an oxoG-clamp in model DNA substrates on the process of 8-oxoG excision by OGG1. Towards that end, we used DNA duplexes modeling OGG1-specific lesions: 8-oxoguanine or an apurinic/apyrimidinic site with either cytidine or the oxoG-clamp in the complementary strand opposite to the lesion. It was revealed that there was neither hydrolysis of the N-glycosidic bond at oxoG nor cleavage of the sugar–phosphate backbone during the reaction between OGG1 and oxoG-clamp-containing duplexes. Possible structural reasons for the absence of OGG1 enzymatic activity were studied via the stopped-flow kinetic approach and molecular dynamics simulations. The base opposite the damage was found to have a critical effect on the formation of the enzyme–substrate complex and the initiation of DNA cleavage. The oxoG-clamp residue prevented the eversion of the oxoG base into the OGG1 active site pocket and impeded the correct convergence of the apurinic/apyrimidinic site of DNA and the attacking nucleophilic group of the enzyme. An obtained three-dimensional model of the OGG1 complex with DNA containing the oxoG-clamp, together with kinetic data, allowed us to clarify the role of the contact of amino acid residues with DNA in the formation of (and rearrangements in) the enzyme–substrate complex. Full article
(This article belongs to the Special Issue DNA Damage and Repair in Health and Diseases)
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Review

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30 pages, 1865 KiB  
Review
Dealkylation of Macromolecules by Eukaryotic α-Ketoglutarate-Dependent Dioxygenases from the AlkB-like Family
by Anastasiia T. Davletgildeeva and Nikita A. Kuznetsov
Curr. Issues Mol. Biol. 2024, 46(9), 10462-10491; https://doi.org/10.3390/cimb46090622 - 20 Sep 2024
Viewed by 1553
Abstract
Alkylating modifications induced by either exogenous chemical agents or endogenous metabolites are some of the main types of damage to DNA, RNA, and proteins in the cell. Although research in recent decades has been almost entirely devoted to the repair of alkyl and [...] Read more.
Alkylating modifications induced by either exogenous chemical agents or endogenous metabolites are some of the main types of damage to DNA, RNA, and proteins in the cell. Although research in recent decades has been almost entirely devoted to the repair of alkyl and in particular methyl DNA damage, more and more data lately suggest that the methylation of RNA bases plays an equally important role in normal functioning and in the development of diseases. Among the most prominent participants in the repair of methylation-induced DNA and RNA damage are human homologs of Escherichia coli AlkB, nonheme Fe(II)/α-ketoglutarate-dependent dioxygenases ABH1–8, and FTO. Moreover, some of these enzymes have been found to act on several protein targets. In this review, we present up-to-date data on specific features of protein structure, substrate specificity, known roles in the organism, and consequences of disfunction of each of the nine human homologs of AlkB. Special attention is given to reports about the effects of natural single-nucleotide polymorphisms on the activity of these enzymes and to potential consequences for carriers of such natural variants. Full article
(This article belongs to the Special Issue DNA Damage and Repair in Health and Diseases)
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