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DNA damage response in vascular endothelial senescence: Implication for radiation-induced cardiovascular diseases
Title: | DNA damage response in vascular endothelial senescence: Implication for radiation-induced cardiovascular diseases |
Authors: | Nagane, Masaki Browse this author | Yasui, Hironobu Browse this author →KAKEN DB | Kuppusamy, Periannan Browse this author | Yamashita, Tadashi Browse this author | Inanami, Osamu Browse this author →KAKEN DB |
Keywords: | radiation-induced cardiovascular disease | endothelial cells (ECs) | nitric oxide (NO) | eNOS | DNA damage response (DDR) |
Issue Date: | 28-Apr-2021 |
Publisher: | Oxford University Press |
Journal Title: | Journal of Radiation Research |
Volume: | 62 |
Issue: | 4 |
Start Page: | 564 |
End Page: | 573 |
Publisher DOI: | 10.1093/jrr/rrab032 |
Abstract: | A post-exposure cohort study in Hiroshima and Nagasaki reported that low-dose exposure to radiation heightened the risk of cardiovascular diseases (CVD), such as stroke and myocardial infarction, by 14-18% per Gy. Moreover, the risk of atherosclerosis in the coronary arteries reportedly increases with radiation therapy of the chest, including breast and lung cancer treatment. Cellular senescence of vascular endothelial cells (ECs) is believed to play an important role in radiation-induced CVDs. The molecular mechanism of age-related cellular senescence is believed to involve genomic instability and DNA damage response (DDR); the chronic inflammation associated with senescence causes cardiovascular damage. Therefore, vascular endothelial cell senescence is believed to induce the pathogenesis of CVDs after radiation exposure. The findings of several prior studies have revealed that ionizing radiation (IR) induces cellular senescence as well as cell death in ECs. We have previously reported that DDR activates endothelial nitric oxide (NO) synthase, and NO production promotes endothelial senescence. Endothelial NO synthase (eNOS) is a major isoform expressed in ECs that maintains cardiovascular homeostasis. Therefore, radiation-induced NO production, a component of the DDR in ECs, may be involved in CVDs after radiation exposure. In this article, we describe the pathology of radiation-induced CVD and the unique radio-response to radiation exposure in ECs. |
Type: | article |
URI: | http://hdl.handle.net/2115/82668 |
Appears in Collections: | 獣医学院・獣医学研究院 (Graduate School of Veterinary Medicine / Faculty of Veterinary Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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