Radiation-Induced Cardiovascular Toxicity: Mechanisms, Prevention, and Treatment

Spetz, Johan; Moslehi, Javid; Sarosiek, Kristopher A.

doi:10.1007/s11936-018-0627-x

Cited by 70 publications

(51 citation statements)

References 71 publications

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“…The removal of undesired or faulty cells by regulated cell death is a fundamental physiological process which is vital for development, immunity and tissue homeostasis. Furthermore, disruption of the programmed cell death pathways can lead to abnormally high or low rates of cell death, and is associated with many of the diseases that constitute the top causes of death worldwide, including cardiovascular, neurodegenerative, pulmonary, renal and hepatic diseases, as well as cancer (Goilav, 2011;Johnstone et al, 2002;Lozano et al, 2012;Lu et al, 2014;Okouchi et al, 2007;Spetz et al, 2018;Su et al, 1997;Wang, 2014;Whelan et al, 2010). Several different modes of programmed cell death have been described in the literature in numerous biological contexts, and the study of these pathways has been instrumental in explaining the diverse biological processes involved in cell loss (Galluzzi et al, 2018).…”

Section: Cell Death Pathways In T Cellsmentioning

confidence: 99%

T Cells and Regulated Cell Death

Spetz

Presser

Sarosiek

2019

International Review of Cell and Molecular Biology

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Cell death plays two major complementary roles in T cell biology: mediating the removal of cells that are targeted by T cells and the removal of T cells themselves. T cells serve as major actors in the adaptive immune response, and function by selectively killing cells which are infected or dysfunctional. The selectivity in the T cell recognition and elimination is a highly regulated feature, which in itself involves the death of both autoreactive T cells and T cells which are unable to recognise threats. Moreover, detection of potential threats will result in the activation and expansion of T cells, which upon resolution of the immune response will need to be eliminated. The culling of these T cells can be executed via a multitude of cell death pathways which are used in context-specific manners. Failure of these processes may result in an accumulation of misdirected or dysfunctional T cells, leading to complications such as autoimmunity or cancer. This review will focus on the role of cell death regulation in the maintenance of T-cell homeostasis as well as T cell-mediated elimination of infected or dysfunctional cells, and will summarize and discuss the current knowledge of the cellular mechanisms which are implicated in these processes.

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Section: Cell Death Pathways In T Cellsmentioning

confidence: 99%

T Cells and Regulated Cell Death

Spetz

Presser

Sarosiek

2019

International Review of Cell and Molecular Biology

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“…Moreover, the risk of cardiovascular complications in patients who received radiotherapy for left breast cancer was significantly higher than the risk in patients who received radiotherapy for right breast cancer [10]. Although the benefit of radiotherapy is obvious, increasing attention has been paid to the cardiac damage induced by radiotherapy, which would suggest limiting the dose and use of radiotherapy in cancer patients [11]. Modern radiotherapy techniques may not have decreased cardiac toxicity even though they have reduced the exposure of the heart to radiation [12].…”

Section: Introductionmentioning

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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“…Investigations into preventing and treating irradiation damage, drug efficacy, and mitigating the effects of irradiation on the pharmacokinetics of drugs, such as 5-fluorouracil, cisplatin, and irinotecan hydrochloride, have been conducted for years (Hsieh et al, 2011;Duan et al, 2015;Tsai et al, 2015;Spetz et al, 2018;Qiao et al, 2019). These studies have observed significant differences in the characteristics of drugs in experimental rats after irradiation exposure.…”

Section: Introductionmentioning

confidence: 99%

Regulation of X-Ray Irradiation on the Activity and Expression Levels of CYP1A2 and CYP2E1 in Rats

Wang

et al. 2020

Front. Pharmacol.

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The objective of this study was to investigate the regulation of X-ray irradiation and its effect on the activity and protein and mRNA expression levels of CYP1A2 and CYP2E1 in rats. Rats were randomly divided into 0 Gy (control), 1 Gy (low-dose irradiation), and 5 Gy (high-dose irradiation) groups. CYP1A2 and CYP2E1 activity was evaluated from changes in pharmacokinetic parameters of caffeine and chlorzoxazone, respectively. The plasma concentrations of the probe drugs were determined by high-performance liquid chromatography (HPLC). Enzyme-linked immunosorbent assay (ELISA) and real-time polymerase chain reaction (PCR) tests were used to analyze the protein and mRNA expression levels of CYP1A2 and CYP2E1, respectively. The AUC 0-12 of caffeine was decreased by 1.7-and 2.5-fold, and the CL was increased by 1.8-and 2.6-fold in the 1 Gy and 5 Gy groups, respectively, compared to the 0 Gy group. The AUC 0-10 of chlorzoxazone was 1.4-and 1.8-fold lower, and the CL was 1.4-and 1.9-fold higher in the 1 Gy and 5 Gy groups, respectively, compared to the 0 Gy group. The metabolism of caffeine and chlorzoxazone increased under X-ray irradiation as CL levels increased and AUC levels decreased, suggesting that CYP1A2 and CYP2E1 activity is enhanced in rats after X-ray irradiation. Compared to that of the 0 Gy group, the protein expression level of CYP1A2 was measured as 28.3% and 38.9% higher in the 1 Gy and 5 Gy groups, respectively. The protein expression level of CYP2E1 was 48.4% higher in the 5 Gy group compared to the 0 Gy group, and there was no statistically significant difference between 0 Gy and 1 Gy. Compared to the 0 Gy group, the mRNA expression level of CYP1A2 was 200% and 856.3% higher in the 1 Gy and 5 Gy group, respectively, whereas the mRNA expression level of CYP2E1 was 89.0% and 192.3% higher in the 1 Gy and 5 Gy groups, respectively. This study reveals significant changes in the activity and protein and mRNA expression levels of CYP1A2 and CYP2E1 in rats after exposure to X-ray irradiation. AnimalsSprague Dawley SPF rats (200 ± 20 g, certificate No. 2007-001) of both sexes were provided by the laboratory animal center at Xi'an Jiaotong University Medical College, China. They were adapted for a week at 23 ± 2°C with a constant humidity level of 55% ± 5% under a cycle of 12 h of dark conditions and given ad libitum Li et al. X-Ray Irradiation and CYP1A2 and CYP2E1 Frontiers in Pharmacology | www.frontiersin.org January 2020 | Volume 10 | Article 1575 2

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Radiation-Induced Cardiovascular Toxicity: Mechanisms, Prevention, and Treatment

Cited by 70 publications

References 71 publications

T Cells and Regulated Cell Death

T Cells and Regulated Cell Death

Oxidative Stress in Radiation-Induced Cardiotoxicity

Regulation of X-Ray Irradiation on the Activity and Expression Levels of CYP1A2 and CYP2E1 in Rats

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