%0 Journal Article
%T Reparative effects after low-dose radiation exposure: Inhibition of atherosclerosis by reducing NETs release.
%A Qu S
%A Qiu X
%A Liu J
%A Feng R
%A Wang Y
%A Dong X
%A Jin Y
%A Liu X
%J Sci Total Environ
%V 947
%N 0
%D 2024 Oct 15
%M 38977089
%F 10.753
%R 10.1016/j.scitotenv.2024.174540
%X <B>OBJECTIVE: </B>The cardiovascular system effects of environmental low-dose radiation exposure on radiation practitioners remain uncertain and require further investigation. The aim of this study was to initially investigate and explore the mechanisms by which low-dose radiation may contribute to atherosclerosis through a multi-omics joint comprehensive basic experiment.<BR><B>METHODS: </B>We used WGCNA and differential analyses to identify shared genes and potential pathways between radiation injury and atherosclerosis sequencing datasets, as well as tissue transcriptome immune infiltration level extrapolation and single-cell transcriptome data correction using the CIBERSORT deconvolution algorithm. Animal models were constructed by combining a high-fat diet with 5 Gy γ-ray whole-body low-dose ionizing radiation. The detection of NETs release was validated by enzyme-linked immunosorbent assay.<BR><B>RESULTS: </B>Analysis reveals shared genes in both datasets of post-irradiation and atherosclerosis, suggesting that immune system neutrophils may be a key node connecting radiation to atherosclerosis. NETs released by neutrophil death can influence the development of atherosclerosis. Animal experiments showed that the number of neutrophils decreased (P < 0.05) and the concentration of NETs reduced after low-dose radiation compared with the control group, and the concentration of NETs significantly increased (P < 0.05) in the HF group. Endothelial plaques were significantly increased in the high-fat feed group and significantly decreased in the low-dose radiation group compared with the control group.<BR><B>CONCLUSIONS: </B>Long-term low-dose ionizing radiation exposure stimulates neutrophils and inhibits their production of NETs, resulting in inhibition of atherosclerosis.