Mechanistic trends and therapeutic targets in Radiation-Induced apoptosis: A bibliometric and translational mapping.

IF 2.4 4区 环境科学与生态学 Q3 BIOLOGY
Radiation and Environmental Biophysics Pub Date : 2026-03-01 Epub Date: 2026-02-02 DOI:10.1007/s00411-026-01194-y
Xiangyu Chen, Yang Hu, Xinghai Yu, Ziwei Zhang, Pu Yang
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引用次数: 0

Abstract

Apoptosis is a central mechanism by which ionizing radiation exerts both therapeutic and toxic biological effects. Despite its pivotal role in radiobiology, the evolving landscape of apoptosis-related radiation research has yet to be systematically mapped from a translational perspective.We conducted a bibliometric and thematic analysis of 4,372 English-language publications (2015–2025) retrieved from the Web of Science Core Collection using the search terms “radiation damage” and “apoptosis.” Co-authorship, keyword, and co-citation networks were visualized using VOSviewer and CiteSpace. Temporal bursts and clustering analysis were performed to identify mechanistic advances and emergent trends relevant to medicinal chemistry. Publications were additionally stratified by radiation modality (IR, UV and EMF).Annual publication volume increased by 15% from 2015 to 2025, with China emerging as the most prolific contributor. However, high-impact citations remained centered in North America and Europe. IR-related studies dominated overall output, while UV- and EMF-associated apoptosis research formed smaller but persistent niches. Research focus has shifted from oxidative stress and canonical DNA damage response pathways (ATM/ATR/PARP) to microenvironment mediated radiosensitivity and nano-enabled drug delivery. Citation-burst analysis highlights ongoing interest in tumor microenvironment modulation, extracellular vesicles, and nanoparticle radiosensitizers. Mechanistic hotspots include STING-mediated DNA sensing, ferroptosis driven mitochondrial destabilization, and DRP1/OPA1-regulated apoptotic commitment. Apoptosis-related radiation research is undergoing a mechanistic and translational shift, with growing relevance for drug discovery, radiosensitization, and biomarker-guided therapy. Cross-disciplinary collaboration and data integration are now critical to accelerating therapeutic innovation in precision radiotherapy.

辐射诱导细胞凋亡的机制趋势和治疗靶点:文献计量学和翻译图谱。
细胞凋亡是电离辐射发挥治疗和毒性生物学作用的主要机制。尽管它在放射生物学中起着关键作用,但凋亡相关辐射研究的发展前景尚未从翻译的角度系统地绘制出来。我们使用搜索词“辐射损伤”和“细胞凋亡”,对从Web of Science核心馆藏中检索的4372篇英语出版物(2015-2025)进行了文献计量学和主题分析。使用VOSviewer和CiteSpace对合著者、关键词和共引网络进行可视化。进行了时间爆发和聚类分析,以确定与药物化学相关的机制进展和新兴趋势。此外,根据辐射方式(IR, UV和EMF)对出版物进行分层。从2015年到2025年,年出版量增长了15%,中国成为最多产的贡献者。然而,高影响力引用仍然集中在北美和欧洲。红外相关的研究占主导地位,而紫外线和电磁场相关的细胞凋亡研究形成了较小但持续的小众。研究重点已从氧化应激和典型DNA损伤反应途径(ATM/ATR/PARP)转移到微环境介导的放射敏感性和纳米药物递送。引文爆发分析强调了对肿瘤微环境调节、细胞外囊泡和纳米粒子放射增敏剂的持续兴趣。机制热点包括sting介导的DNA传感、铁下垂驱动的线粒体不稳定以及DRP1/ opa1调节的凋亡承诺。与细胞凋亡相关的放射研究正经历着机制和转化的转变,与药物发现、放射增敏和生物标志物引导治疗的相关性越来越大。跨学科合作和数据整合现在对于加速精确放疗的治疗创新至关重要。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
4.00
自引率
5.90%
发文量
53
审稿时长
>36 weeks
期刊介绍: This journal is devoted to fundamental and applied issues in radiation research and biophysics. The topics may include: Biophysics of ionizing radiation: radiation physics and chemistry, radiation dosimetry, radiobiology, radioecology, biophysical foundations of medical applications of radiation, and radiation protection. Biological effects of radiation: experimental or theoretical work on molecular or cellular effects; relevance of biological effects for risk assessment; biological effects of medical applications of radiation; relevance of radiation for biosphere and in space; modelling of ecosystems; modelling of transport processes of substances in biotic systems. Risk assessment: epidemiological studies of cancer and non-cancer effects; quantification of risk including exposures to radiation and confounding factors Contributions to these topics may include theoretical-mathematical and experimental material, as well as description of new techniques relevant for the study of these issues. They can range from complex radiobiological phenomena to issues in health physics and environmental protection.
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