Ionizing radiation and heart risks

Bhattacharya, Souparno; Asaithamby, Aroumougame

doi:10.1016/j.semcdb.2016.01.045

Cited by 60 publications

(47 citation statements)

References 146 publications

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“…One of the targets of ionizing radiation that is linked to radiation-induced CVD is the endothelium (Little et al, 2008;Hildebrandt, 2010). Exposure of endothelial cells to radiation results in endothelial cell dysfunction (Bhattacharya and Asaithamby, 2016), promoting the development and progression of atherosclerosis (Vita and Keaney, 2002;Widmer and Lerman, 2014). Atherosclerosis is a complex process in which arteries narrow due to plaque formation, a process characterized by DNA damage, inflammation, senescence and apoptosis (Yu et al, 2012).…”

Section: Introductionmentioning

confidence: 99%

Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction

et al. 2020

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Background and Purpose: Up to 50-60% of all cancer patients receive radiotherapy as part of their treatment strategy. However, the mechanisms accounting for increased vascular risks after irradiation are not completely understood. Mitochondrial dysfunction has been identified as a potential cause of radiation-induced atherosclerosis.Materials and Methods: Assays for apoptosis, cellular metabolism, mitochondrial DNA content, functionality and morphology were used to compare the response of endothelial cells to a single 2 Gy dose of X-rays under basal conditions or after pharmacological treatments that either reduced (EtBr) or increased (rosiglitazone) mitochondrial content.Results: Exposure to ionizing radiation caused a persistent reduction in mitochondrial content of endothelial cells. Pharmacological reduction of mitochondrial DNA content rendered endothelial cells more vulnerable to radiation-induced apoptosis, whereas rosiglitazone treatment increased oxidative metabolism and redox state and decreased the levels of apoptosis after irradiation.Conclusion: Pre-existing mitochondrial damage sensitizes endothelial cells to ionizing radiation-induced mitochondrial dysfunction. Rosiglitazone protects endothelial cells from the detrimental effects of radiation exposure on mitochondrial metabolism and oxidative stress. Thus, our findings indicate that rosiglitazone may have potential value as prophylactic for radiation-induced atherosclerosis.

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Section: Introductionmentioning

confidence: 99%

Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction

et al. 2020

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“…Indeed, exposure of the vascular endothelium to IR can result in endothelial cell dysfunction (Bhattacharya and Asaithamby, 2016), a well-established cardiovascular risk factor that promotes the development and progression of atherosclerosis (Vita and Keaney, 2002; Widmer and Lerman, 2014). Although the mechanisms of radiation-induced CVD are far from being understood, inflammatory processes seem to be involved.…”

Section: Introductionmentioning

confidence: 99%

Functional Gene Analysis Reveals Cell Cycle Changes and Inflammation in Endothelial Cells Irradiated with a Single X-ray Dose

et al. 2017

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Background and Purpose: Epidemiological data suggests an excess risk of cardiovascular disease (CVD) at low doses (0.05 and 0.1 Gy) of ionizing radiation (IR). Furthermore, the underlying biological and molecular mechanisms of radiation-induced CVD are still unclear. Because damage to the endothelium could be critical in IR-related CVD, this study aimed to identify the effects of radiation on immortalized endothelial cells in the context of atherosclerosis.Material and Methods: Microarrays and RT-qPCR were used to compare the response of endothelial cells irradiated with a single X-ray dose (0.05, 0.1, 0.5, 2 Gy) measured after various post-irradiation (repair) times (1 day, 7 days, 14 days). To consolidate and mechanistically support the endothelial cell response to X-ray exposure identified via microarray analysis, DNA repair signaling (γH2AX/TP53BP1-foci quantification), cell cycle progression (BrdU/7AAD flow cytometric analysis), cellular senescence (β-galactosidase assay with CPRG and IGFBP7 quantification) and pro-inflammatory status (IL6 and CCL2) was assessed.Results: Microarray results indicated persistent changes in cell cycle progression and inflammation. Cells underwent G1 arrest in a dose-dependent manner after high doses (0.5 and 2 Gy), which was compensated by increased proliferation after 1 week and almost normalized after 2 weeks. However, at this point irradiated cells showed an increased β-Gal activity and IGFBP7 secretion, indicative of premature senescence. The production of pro-inflammatory cytokines IL6 and CCL2 was increased at early time points.Conclusions: IR induces pro-atherosclerotic processes in endothelial cells in a dose-dependent manner. These findings give an incentive for further research on the shape of the dose-response curve, as we show that even low doses of IR can induce premature endothelial senescence at later time points. Furthermore, our findings on the time- and dose-dependent response regarding differentially expressed genes, cell cycle progression, inflammation and senescence bring novel insights into the underlying molecular mechanisms of the endothelial response to X-ray radiation. This may in turn lead to the development of risk-reducing strategies to prevent IR-induced CVD, such as the use of cell cycle modulators and anti-inflammatory drugs as radioprotectors and/or radiation mitigators.

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“…IL-4 and Oxidative Stress. IL-4 has long been considered to be an effective fibrogenic factor because it can induce the synthesis of ECM protein, collagen, and fibronectin[59]. Recent studies have shown that IL-4 and IL-13 are of…”

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confidence: 99%

Oxidative Stress in Radiation-Induced Cardiotoxicity

Zhang

Yang

Liu

et al. 2020

Oxidative Medicine and Cellular Longevity

115

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There is a distinct increase in the risk of heart disease in people exposed to ionizing radiation (IR). Radiation-induced heart disease (RIHD) is one of the adverse side effects when people are exposed to ionizing radiation. IR may come from various forms, such as diagnostic imaging, radiotherapy for cancer treatment, nuclear disasters, and accidents. However, RIHD was mainly observed after radiotherapy for chest malignant tumors, especially left breast cancer. Radiation therapy (RT) has become one of the main ways to treat all kinds of cancer, which is used to reduce the recurrence of cancer and improve the survival rate of patients. The potential cause of radiation-induced cardiotoxicity is unclear, but it may be relevant to oxidative stress. Oxidative stress, an accumulation of reactive oxygen species (ROS), disrupts intracellular homeostasis through chemical modification and damages proteins, lipids, and DNA; therefore, it results in a series of related pathophysiological changes. The purpose of this review was to summarise the studies of oxidative stress in radiotherapy-induced cardiotoxicity and provide prevention and treatment methods to reduce cardiac damage.

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Ionizing radiation and heart risks

Cited by 60 publications

References 146 publications

Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction

Rosiglitazone Protects Endothelial Cells From Irradiation-Induced Mitochondrial Dysfunction

Functional Gene Analysis Reveals Cell Cycle Changes and Inflammation in Endothelial Cells Irradiated with a Single X-ray Dose

Oxidative Stress in Radiation-Induced Cardiotoxicity

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