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Radiation-Induced Cellular and Molecular Responses
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Radiation-Induced Cellular and Molecular Responses

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

Deadline for manuscript submissions: 31 August 2026 | Viewed by 15263

Special Issue Editor

Dr. Carlo Aprile

E-Mail Website
Guest Editor
IRCCS Fondazione Policlinico San Matteo, Nuclear Medicine Unit, I-27100 Pavia, Italy
Interests: molecular imaging; internal radiotherapy; radiopharmacology; diabetes; tumors; space radiobiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Radiation exposure, whether from environmental sources, medical treatments, or occupational hazards, has profound effects on biological systems. The impact of radiation on cells and tissues can lead to complex molecular responses, driving efforts to understand these processes for better therapeutic and protective strategies.

This Special Issue invites original research and review articles that delve into molecular pathways, including DNA damage and repair, signal transduction, apoptosis, autophagy, and cellular senescence induced by radiation. We also welcome studies on the role of non-coding RNAs, epigenetic modifications, and molecular markers in radiation response. Research on the development of novel radioprotective agents and strategies to mitigate radiation-induced damage is particularly encouraged. By gathering cutting-edge research, this Special Issue aims to provide comprehensive insights into the molecular underpinnings of radiation effects, contributing to the development of more effective therapeutic interventions and protective measures.

We invite contributions from researchers across the fields of molecular biology, biochemistry, oncology, and related disciplines to enhance our understanding of radiation-induced biological responses and their implications for human health.

Dr. Carlo Aprile
Guest Editor

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Current Issues in Molecular Biology is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2200 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • radiation
  • radiobiology
  • space radiobiology
  • heavy ions carcinogenesis
  • LinearNonTreshold
  • radionuclide therapy
  • alpha emitters
  • beta emitters
  • radiobiology

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Published Papers (4 papers)

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Research

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15 pages, 4825 KB  
Article
Radiosensitization Effect of PARP Inhibitor Talazoparib Involves Decreasing Mitochondrial Membrane Potential and Induction of Cellular Senescence
by Barkha Saraswat, Ankitha Vadi Velu, Zhongming Gao, Zongxiang Zhang, Haoyang Zhu, Ying Tong and Mitsuko Masutani
Curr. Issues Mol. Biol. 2025, 47(11), 908; https://doi.org/10.3390/cimb47110908 - 1 Nov 2025
Viewed by 793
Abstract
Poly (ADP-ribose) polymerase (PARP) inhibitors (PARPis) with radiation therapy can enhance the sensitivity of cancer cells by inhibiting DNA repair pathways. To determine the most suitable PARP inhibitor for radiosensitization in cancer cells, we compared various types of clinically used PARPis in lung [...] Read more.
Poly (ADP-ribose) polymerase (PARP) inhibitors (PARPis) with radiation therapy can enhance the sensitivity of cancer cells by inhibiting DNA repair pathways. To determine the most suitable PARP inhibitor for radiosensitization in cancer cells, we compared various types of clinically used PARPis in lung cancer A549 cells. We found that most PARP inhibitors showed radiosensitization effects on A549 cells. ER10 values for talazoparib, olaparib rucaparib, ABT888 and niraparib were 1.5, 1.8, 2.8, 1.4, and 1.4, respectively. Talazoparib showed a radiosensitization effect at its lowest concentration. Talazoparib is a potent PARP inhibitor and has been used in clinical settings for several types of cancer as an anti-cancer agent. We thus focused on how talazoparib causes radiosensitization in lung cancer A549 cells. As a result of the combination of talazoparib and γ-irradiation, we observed an increased level of cellular senescence accompanied by a decrease in mitochondrial membrane potential. When the p21 gene was knocked down, both the decrease in mitochondrial membrane potential and senescence level were attenuated, suggesting that p21 is involved in senescence induction after γ-irradiation combined with talazoparib treatment. Taken together, we showed that PARP inhibitor talazoparib treatment in combination with γ-irradiation causes cellular senescence in lung cancer cells, involving p21 function. Full article
(This article belongs to the Special Issue Radiation-Induced Cellular and Molecular Responses)
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17 pages, 2112 KB  
Article
Mitigation of 3.5 GHz Electromagnetic Field-Induced BV2 Microglial Cytotoxicity by Polydeoxyribonucleotide
by Shailashree Pachhapure, Amila Mufida, Qun Wei, Jong-Soon Choi and Byeong-Churl Jang
Curr. Issues Mol. Biol. 2025, 47(6), 386; https://doi.org/10.3390/cimb47060386 - 22 May 2025
Viewed by 1798
Abstract
Emerging evidence highlights the biological risks associated with electromagnetic fields (EMFs) generated by electronic devices. The toxic effects and mechanisms induced by exposure to EMFs on microglial cells and natural substances that inhibit them are limited to date. Here, we investigated whether exposure [...] Read more.
Emerging evidence highlights the biological risks associated with electromagnetic fields (EMFs) generated by electronic devices. The toxic effects and mechanisms induced by exposure to EMFs on microglial cells and natural substances that inhibit them are limited to date. Here, we investigated whether exposure to 3.5 GHz EMF radiation, potentially generated by smartphones working in 5G communication or cooking using microwave ovens, affects the growth of BV2 mouse microglial cells and polydeoxyribonucleotide (PDRN), a DNA preparation derived from salmon sperm, inhibits it. Of note, exposure to 3.5 GHz EMF radiation for 2 h markedly inhibited the growth and triggered apoptosis in BV2 cells, characterized by the reduced number of surviving cells, increased genomic DNA fragmentation, increased reactive oxygen species (ROS) levels, and altered phosphorylation and expression levels of JNK-1/2, p38 MAPK, ERK-1/2, eIF-2α, and procaspase-9. Pharmacological inhibition studies revealed that JNK-1/2 and p38 MAPK activation and ROS generation were crucial for 3.5 GHz EMF-induced BV2 cytotoxicity. Of interest, PDRN effectively countered these effects by inhibiting the activation of JNK-1/2, p38 MAPK, and caspase-9, and the production of ROS, although it did not affect eIF-2 phosphorylation. In conclusion, this study is the first to report that PDRN protects against 3.5 GHz EMF-induced toxicities in BV2 microglial cells, and PDRN’s protective effects on 3.5 GHz EMF-induced BV2 cytotoxicity are mediated primarily by modulating ROS, JNK-1/2, p38 MAPK, and caspase-9. Full article
(This article belongs to the Special Issue Radiation-Induced Cellular and Molecular Responses)
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Review

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22 pages, 861 KB  
Review
A Review of Ionizing Radiation-Induced Senescence of Bone Marrow Mesenchymal Stem/Stromal Cells: Mechanisms and Therapeutic Strategies
by Xiaoliang Li, Maoshan Chen, Yangyang Zhang, Jiuxuan Li, Lixin Xiang, Yanni Xiao, Yang Xiang, Li Chen, Qian Ran and Zhongjun Li
Curr. Issues Mol. Biol. 2026, 48(2), 196; https://doi.org/10.3390/cimb48020196 - 10 Feb 2026
Viewed by 30
Abstract
Bone marrow mesenchymal stem/stromal cells (BM-MSCs) are important components of bone marrow, possessing multipotent differentiation potential and the ability to support hematopoiesis. Exposure to ionizing radiation (IR) induces cellular damage in BM-MSCs, such as DNA lesions and mitochondrial dysfunction. Despite their relative radioresistance, [...] Read more.
Bone marrow mesenchymal stem/stromal cells (BM-MSCs) are important components of bone marrow, possessing multipotent differentiation potential and the ability to support hematopoiesis. Exposure to ionizing radiation (IR) induces cellular damage in BM-MSCs, such as DNA lesions and mitochondrial dysfunction. Despite their relative radioresistance, most surviving BM-MSCs enter senescence post-irradiation. This senescent state disrupts the bone marrow niche, impairs stem cell proliferation and differentiation, and contributes to acute radiation syndrome (ARS) and myelosuppression. To clarify the impact of IR on BM-MSCs, this review systematically summarizes the general mechanisms of radiation-induced cellular senescence, examines the effects of different radiation types (e.g., gamma rays, X-rays, and heavy-ion radiation) and doses on BM-MSCs senescence, and outlines senotherapeutic strategies targeting BM-MSCs senescence. The analysis indicates that the senescence of BM-MSCs caused by IR is type- and dose-dependent. The review identifies key factors in IR-induced BM-MSCs senescence to guide targeted interventions, highlighting the need for future studies to elucidate the underlying mechanisms of IR-induced BM-MSCs senescence. Full article
(This article belongs to the Special Issue Radiation-Induced Cellular and Molecular Responses)
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15 pages, 744 KB  
Review
Molecular Insights into Radiation Effects and Protective Mechanisms: A Focus on Cellular Damage and Radioprotectors
by Blanca Ibáñez, Ana Melero, Alegría Montoro, Nadia San Onofre and Jose M. Soriano
Curr. Issues Mol. Biol. 2024, 46(11), 12718-12732; https://doi.org/10.3390/cimb46110755 - 9 Nov 2024
Cited by 19 | Viewed by 11866
Abstract
Ionizing radiation has been a critical tool in various fields, such as medicine, agriculture, and energy production, since its discovery in 1895. While its applications—particularly in cancer treatment and diagnostics—offer significant benefits, ionizing radiation also poses risks due to its potential to cause [...] Read more.
Ionizing radiation has been a critical tool in various fields, such as medicine, agriculture, and energy production, since its discovery in 1895. While its applications—particularly in cancer treatment and diagnostics—offer significant benefits, ionizing radiation also poses risks due to its potential to cause molecular and cellular damage. This damage can occur through the direct ionization of biological macromolecules, such as deoxyribonucleic acid (DNA), or indirectly through the radiolysis of water, which generates reactive oxygen species (ROS) that further damage cellular components. Radioprotectors, compounds that protect against radiation-induced damage, have been extensively researched since World War II. These agents work by enhancing DNA repair, scavenging free radicals, and boosting antioxidant defenses, thereby protecting healthy tissues. Furthermore, some radioprotective agents also stimulate DNA repair mechanisms even after radiation exposure, aiding in recovery from radiation-induced damage. This article explores the molecular mechanisms of radiation-induced damage, focusing on both direct and indirect effects on DNA, and discusses the role of radioprotectors, their mechanisms of action, and recent advancements in the field. The findings underscore the importance of developing effective radioprotective strategies, particularly in medical and industrial settings, where radiation exposure is prevalent. Full article
(This article belongs to the Special Issue Radiation-Induced Cellular and Molecular Responses)
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