ArticlePloS one2022
A systems radiation biology approach to unravel the role of chronic low-dose-rate gamma-irradiation in inducing premature senescence in endothelial cells.
Article in PloS one, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Biological effects of conventional and ultra high dose rate radiation in human cells.Scientific reports · 2026Article
- Cellular responses to targeted radionuclide therapy: rethinking radiobiology under continuous low dose rates.Frontiers in oncology · 2026Review
- Drosophila melanogaster: an old and future ally to radiobiology.Journal of radiation research · 2025Review
- An In-depth Analysis of the Adverse Effects of Ionizing Radiation Exposure on Cardiac Catheterization Staffs.Current radiopharmaceuticals · 2024Review
- Tissue Reactions and Mechanism in Cardiovascular Diseases Induced by Radiation.International journal of molecular sciences · 2022Review
- Radiation dose rate effects: what is new and what is needed?Radiation and environmental biophysics · 2022Review
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Authors and funding
18 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeThe aim of this study was to explore the effects of chronic low-dose-rate gamma-radiation at a multi-scale level. The specific objective was to obtain an overall view of the endothelial cell response, by integrating previously published data on different cellular endpoints and highlighting possible different mechanisms underpinning radiation-induced senescence. MATERIALS AND
methodsDifferent datasets were collected regarding experiments on human umbilical vein endothelial cells (HUVECs) which were chronically exposed to low dose rates (0, 1.4, 2.1 and 4.1 mGy/h) of gamma-rays until cell replication was arrested. Such exposed cells were analyzed for different complementary endpoints at distinct time points (up to several weeks), investigating cellular functions such as proliferation, senescence and angiogenic properties, as well as using transcriptomics and proteomics profiling. A mathematical model was proposed to describe proliferation and senescence.
resultsSimultaneous ceasing of cell proliferation and senescence onset as a function of time were well reproduced by the logistic growth curve, conveying shared equilibria between the two endpoints. The combination of all the different endpoints investigated highlighted a dose-dependence for prematurely induced senescence. However, the underpinning molecular mechanisms appeared to be dissimilar for the different dose rates, thus suggesting a more complex scenario.
conclusionsThis study was conducted integrating different datasets, focusing on their temporal dynamics, and using a systems biology approach. Results of our analysis highlight that different dose rates have different effects in inducing premature senescence, and that the total cumulative absorbed dose also plays an important role in accelerating endothelial cell senescence.
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