ArticlePloS one2013
The PI3K/Akt/mTOR pathway is implicated in the premature senescence of primary human endothelial cells exposed to chronic radiation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
57 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.
- Ionising radiation and cardiovascular disease: systematic review and meta-analysis.BMJ (Clinical research ed.) · 2023Pooled it
- Long-Term Trends and Prognosis in Cardiovascular Mortality in the Kazakhstani Population Living Around the Semipalatinsk Nuclear Test Site.International journal of environmental research and public health · 2026Article
- Exploiting cellular senescence in hematologic malignancies.Translational oncology · 2026Review
- Adverse Outcome Pathways Applied to Space Radiation Research.Environmental and molecular mutagenesis · 2025Review
- Dendrobium officinale Kimura & Migo polysaccharide ameliorates skin photoaging by promoting angiogenesis.Scientific reports · 2025Article
- Mesenchymal stem cells and their exosomes: a novel approach to skin regeneration via signaling pathways activation.Journal of molecular histology · 2025Review
- Radiation-Induced Macrovessel/Microvessel Disease.Arteriosclerosis, thrombosis, and vascular biology · 2024Review
- Generation of a conditional cellular senescence model using proximal tubule cells and fibroblasts from human kidneys.Cell death discovery · 2024Article
- Revisiting an Inverse Dose-Fractionation Effect of Ionizing Radiation Exposure for Ischemic Heart Disease: Insights from Recent Studies.Radiation research · 2024Review
- Differential gene expression and miRNA regulatory network in coronary slow flow.Scientific reports · 2024Article
- Updated Estimates of Radiation Risk for Cancer and Cardiovascular Disease: Implications for Cardiology Practice.Journal of clinical medicine · 2024Review
- MicroRNAs-associated with FOXO3 in cellular senescence and other stress responses.Biogerontology · 2024Review
- Low-Dose Non-Targeted Effects and Mitochondrial Control.International journal of molecular sciences · 2023Review
- 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
- Article
- Article
- Molecular mechanisms and cardiovascular implications of cancer therapy-induced senescence.Pharmacology & therapeutics · 2021Review
- Vascular Endothelial Senescence: Pathobiological Insights, Emerging Long Noncoding RNA Targets, Challenges and Therapeutic Opportunities.Frontiers in physiology · 2021Review
- Ionizing radiation-induced circulatory and metabolic diseases.Environment international · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The etiology of radiation-induced cardiovascular disease (CVD) after chronic exposure to low doses of ionizing radiation is only marginally understood. We have previously shown that a chronic low-dose rate exposure (4.1 mGy/h) causes human umbilical vein endothelial cells (HUVECs) to prematurely senesce. We now show that a dose rate of 2.4 mGy/h is also able to trigger premature senescence in HUVECs, primarily indicated by a loss of growth potential and the appearance of the senescence-associated markers ß-galactosidase (SA-ß-gal) and p21. In contrast, a lower dose rate of 1.4 mGy/h was not sufficient to inhibit cellular growth or increase SA-ß-gal-staining despite an increased expression of p21. We used reverse phase protein arrays and triplex Isotope Coded Protein Labeling with LC-ESI-MS/MS to study the proteomic changes associated with chronic radiation-induced senescence. Both technologies identified inactivation of the PI3K/Akt/mTOR pathway accompanying premature senescence. In addition, expression of proteins involved in cytoskeletal structure and EIF2 signaling was reduced. Age-related diseases such as CVD have been previously associated with increased endothelial cell senescence. We postulate that a similar endothelial aging may contribute to the increased rate of CVD seen in populations chronically exposed to low-dose-rate radiation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.