Category Ranking

98%

Total Visits

921

Avg Visit Duration

2 minutes

Citations

20

Article Abstract

The impact of ionizing radiation (IR) with induction of various DNA damage is based not only on genetic but also on epigenetic effects. Epigenetic modifications determine the chromatin structure and DNA accessibility, thereby regulating cellular functions through the expression of individual genes or entire groups of genes. However, the influence of DNA repair processes on the restoration of local chromatin structures and global nuclear architectures is still insufficiently understood. In multicellular organisms, epigenetic mechanisms control diverse cellular functions of specific cell types through precise temporal and spatial regulation of gene expression and silencing. How altered epigenetic mechanisms regulate the pathophysiological function of cells, tissues, and ultimately entire organs following IR exposure remains to be investigated in detail. Radiation-induced epigenetic processes are particularly critical for immature cell populations such as tissue-specific stem and progenitor cells during development and differentiation of organ tissues. Genome-wide patterns of DNA and histone modifications are established cell types-specifically during the development and differentiation of organ tissues but can also be fundamentally altered in adult organism by stress responses, such as radiation-induced DNA damage. Following IR exposure, epigenetic factors are not always fully restored to their original state, resulting in epigenetic dysfunction that causes cells to lose their original identity and function. Moreover, severe radiation-induced DNA damage can induce premature senescence of cells in complex tissues, which ultimately leads to signs of aging and age-related diseases such as cancer. In this work, we provide an overview of the most important epigenetic changes following IR exposure and their pathophysiological significance for the development of acute and chronic radiation reactions.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC12372155PMC
http://dx.doi.org/10.3390/epigenomes9030029DOI Listing

Publication Analysis

Top Keywords

dna damage
12
ionizing radiation
8
epigenetic
8
cellular functions
8
epigenetic mechanisms
8
tissues ultimately
8
development differentiation
8
differentiation organ
8
organ tissues
8
radiation-induced dna
8

Similar Publications

Hematopoietic malignancies (HM) represent the most common form of pediatric cancer with lymphoid malignancies being the predominant subtype in kids. The majority of lymphoid malignancies are proposed to occur sporadically with environmental, infectious and inflammatory triggers impacting oncogenesis in ways that are not yet fully understood. With the increased adoption of germline genetic testing in children with cancer, genetic predisposition to lymphoid malignancies is now recognized as an important aspect of clinical care and research.

View Article and Find Full Text PDF

Neural tumors represent diverse malignancies with distinct molecular profiles and present particular challenges due to the blood-brain barrier, heterogeneous molecular etiology including epigenetic dysregulation, and the affected organ's critical nature. KCC-07, a selective and blood-brain barrier penetrable MBD2 (methyl CpG binding domain protein 2) inhibitor, can suppress tumor development by inducing p53 signaling, proven only in medulloblastoma. Here we demonstrate KCC-07 treatment's application to other neural tumors.

View Article and Find Full Text PDF

The immune system uses a variety of DNA sensors, including endo-lysosomal Toll-like receptors 9 (TLR9) and cytosolic DNA sensor cyclic GMP-AMP (cGAMP) synthase (cGAS). These sensors activate immune responses by inducing the production of a variety of cytokines, including type I interferons (IFN). Activation of cGAS requires DNA-cGAS interaction.

View Article and Find Full Text PDF

Glioblastoma (GBM) is a lethal brain tumor with limited therapeutic options. Temozolomide (TMZ), a standard-of-care chemotherapeutic agent, exerts its cytotoxicity by alkylating DNA, which triggers a DNA damage response and depletes ATP and NAD. However, TMZ also releases the byproduct 4-amino-5-imidazole carboxamide (AIC), which is believed to be a benign metabolite.

View Article and Find Full Text PDF

Circ_IGF2BP1/miR-885-3p/TK1 axis regulates the malignant phenotype and chemotherapeutic resistance of lung adenocarcinoma cells via DNA damage and apoptosis.

Int J Biol Macromol

September 2025

Department of Thoracic Surgery, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi, 563000, Guizhou, China; The Public Experimental Center of Medicine, Affiliated Hospital of Zunyi Medical University, 149 Dalian Road, Zunyi, 563000, Guizhou, China. Electronic address: kexixian@z

Chemotherapy resistance in lung adenocarcinoma (LUAD) limits clinical efficacy. In this study, we first established circ_IGF2BP1 knockdown models in LUAD cells (A549 and H1299). Using dual-luciferase reporter assays, functional analyses, and miR-885-3p rescue experiments, we demonstrated that circ_IGF2BP1 promotes LUAD cell proliferation, migration, and invasion by directly targeting miR-885-3p.

View Article and Find Full Text PDF