[1]王梦迪 李敏 曹璐 许赪 欧丹 王舒蓓 陈佳艺.心血管内皮细胞放射性损伤机制的研究进展[J].心血管病学进展,2021,(2):101.[doi:10.16806/j.cnki.issn.1004-3934.2021.02.002]
 WANG Mengdi,LI Min,CAO Lu,et al.Mechanism of Radiation-induced Cardiovascular Endothelial Cell Injury[J].Advances in Cardiovascular Diseases,2021,(2):101.[doi:10.16806/j.cnki.issn.1004-3934.2021.02.002]
点击复制

心血管内皮细胞放射性损伤机制的研究进展()
分享到:

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2021年2期
页码:
101
栏目:
综述
出版日期:
2021-02-25

文章信息/Info

Title:
Mechanism of Radiation-induced Cardiovascular Endothelial Cell Injury
作者:
王梦迪 李敏 曹璐 许赪 欧丹 王舒蓓 陈佳艺
 (上海交通大学医学院附属瑞金医院放射治疗科,上海 200025)
Author(s):
WANG MengdiLI MinCAO LuXU ChengOU DanWANG ShubeiCHEN Jiayi
(Department of Radiation Oncology,Ruijin Hospital,Shanghai Jiaotong University School of Medicine,Shanghai 200025,China)
关键词:
血管内皮细胞电离辐射机制
Keywords:
Vascular endothelial cell Ionizing radiation Mechanism
DOI:
10.16806/j.cnki.issn.1004-3934.2021.02.002
摘要:
放射性心脏疾病已成为胸部放射治疗患者非恶性肿瘤死亡的主要原因之一。心血管内皮细胞损伤是放射性心脏损伤的初始靶点,因此研究心血管内皮细胞放射性损伤机制对于改善放射治疗患者预后具有重要的临床价值。现综述放射相关内皮细胞可能的损伤机制及潜在的保护策略,以期为临床预防或干预放射性心脏疾病提供新思路。
Abstract:
Radiation-induced heart disease (RIHD) has become one of the major causes of non-malignancy death among patients treated with thoracic radiotherapy. Cardiovascular endothelial cell injury is the initial pathogenesis of RIHD. Therefore,exploring the mechanism of radiation-induced cardiovascular endothelial cell injury has important clinical value to improve the prognosis of cardiovascular diseases in radiation-exposed individuals. This article reviews the recent researches on possible mechanism of radiation-induced endothelial cell injury and potential protective strategies,in order to provide new ideas for clinical prevention or intervention of RIHD

参考文献/References:




[1] Andratschke N,Maurer J,Molls M,et al. Late radiation-induced heart disease after radiotherapy. Clinical importance,radiobiological mechanisms and strategies of prevention[J]. Radiother Oncol,2011,100(2):160-166.

[2] Baker JE,Moulder JE,Hopewell JW. Radiation as a risk factor for cardiovascular disease[J]. Antioxid Redox Signal,2011,15(7):1945-1956.

[3] Tapio S. Using proteomics to explore the effects of radiation on the heart - impacts for medicine[J]. Expert Rev Proteomics,2017,14(4):277-279.

[4] Seemann I,Gabriels K,Visser NL,et al. Irradiation induced modest changes in murine cardiac function despite progressive structural damage to the myocardium and microvasculature[J]. Radiother Oncol,2012,103(2):143-150.

[5] Darby SC,Cutter DJ,Boerma M,et al. Radiation-related heart disease:current knowledge and future prospects[J]. Int J Radiat Oncol Biol Phys,2010,76(3):656-665.

[6] Preidl RHM,M?bius P,Weber M,et al. Long-term endothelial dysfunction in irradiated vessels:An immunohistochemical analysis[J]. Strahlenther Onkol,2019,195(1):52-61.

[7] Mathias D,Mitchel RE,Barclay M,et al. Low-dose irradiation affects expression of inflammatory markers in the heart of ApoE-/-mice[J]. PLoS One,2015,10(3):e0119661.

[8] Patties I,Haagen J,D?rr W,et al. Late inflammatory and thrombotic changes in irradiated hearts of C57BL/6 wild-type and atherosclerosis-prone ApoE-deficient mice[J]. Strahlenther Onkol,2015,191(2):172-179.

[9] Baselet B,Sonveaux P,Baatout S,et al. Pathological effects of ionizing radiation:endothelial activation and dysfunction[J]. Cell Mol Life Sci,2019,76(4):699-728.

[10] Baselet B,Belmans N,Coninx E,et al. Functional gene analysis reveals cell cycle changes and inflammation in endothelial cells irradiated with a single X-ray dose[J]. Front Pharmacol,2017,8:213.

[11] Azimzadeh O,Sievert W,Sarioglu H,et al. Integrative proteomics and targeted transcriptomics analyses in cardiac endothelial cells unravel mechanisms of long-term radiation-induced vascular dysfunction[J]. J Proteome Res,2015,14(2):1203-1219.

[12] Hildebrandt G,Maggiorella L,R?del F,et al. Mononuclear cell adhesion and cell adhesion molecule liberation after X-irradiation of activated endothelial cells in vitro[J]. Int J Radiat Biol,2002,78(4):315-325.

[13] Kern PM,Keilholz L,Forster C,et al. Low-dose radiotherapy selectively reduces adhesion of peripheral blood mononuclear cells to endothelium in vitro[J]. Radiother Oncol,2000,54(3):273-282.

[14] Subramanian V,Seemann I,Merl-Pham J,et al. Role of TGF beta and PPAR alpha signaling pathways in radiation response of locally exposed heart:integrated global transcriptomics and proteomics analysis[J]. J Proteome Res,2017,16(1):307-318.

[15] Sniegon I,Prie? M,Heger J,et al. Endothelial mesenchymal transition in hypoxic microvascular endothelial cells and paracrine induction of cardiomyocyte apoptosis are mediated via TGFβ1/SMAD signaling[J]. Int J Mol Sci,2017,18(11):2290.

[16] Soroush F,Tang Y,Zaidi HM,et al. PKCδ inhibition as a novel medical countermeasure for radiation-induced vascular damage[J].FASEB J,2018,32(12):6436-6344.

[17] Christersdottir T,Pirault J,Gister? A,et al. Prevention of radiotherapy-induced arterial inflammation by interleukin-1 blockade[J]. Eur Heart J,2019,40(30):2495-2503.

[18] Chen B,Lu Y,Chen Y,et al. The role of Nrf2 in oxidative stress-induced endothelial injuries[J]. J Endocrinol,2015,225(3):R83-R99.

[19] Bohlen HG. Nitric oxide and the cardiovascular system[J]. Compr Physiol,2011,5(2):803-828.

[20] Zhang ZY,Li Y,Li R,et al. Tetrahydrobiopterin protects against radiation-induced growth inhibition in H9c2 cardiomyocytes[J]. Chin Med J(Engl),2016,129(22):2733.

[21] Pathak R,Cheema AK,Boca SM,et al. Modulation of radiation response by the tetrahydrobiopterin pathway[J]. Antioxidants,2015,4(1):68-81.

[22] Nagane M,Yasui H,Sakai Y,et al. Activation of eNOS in endothelial cells exposed to ionizing radiation involves components of the DNA damage response pathway[J]. Biochem Biophys Res Commun,2015,456(1):541-546.

[23] Leucker TM,Ge ZD,Procknow J,et al. Impairment of endothelial-myocardial interaction increases the susceptibility of cardiomyocytes to ischemia/reperfusion injury[J]. PloS one,2013,8(7):e70088.

[24] Guillonneau M,Paris F,Dutoit S,et al. Oxidative stress disassembles the p38/NPM/PP2A complex,which leads to modulation of nucleophosmin-mediated signaling to DNA damage response[J]. FASEB J,2016,30(8):2899-2914.

[25] Lafargue A,Degorre C,Corre I,et al. Ionizing radiation induces long-term senescence in endothelial cells through mitochondrial respiratory complex II dysfunction and superoxide generation[J]. Free Radic Biol Med,2017,108:750-759.

[26] Hu S,Gao Y,Zhou H,et al. New insight into mitochondrial changes in vascular endothelial cells irradiated by gamma ray[J]. Int J Radiat Biol,2017,93(5):470-476.

[27] Ribeiro-Rodrigues TM,Laundos TL,Pereira-Carvalho R,et al. Exosomes secreted by cardiomyocytes subjected to ischaemia promote cardiac angiogenesis[J]. Cardiovasc Res,2017,113(11):1338-1350.

[28] Davidson SM,Takov K,Yellon DM. Exosomes and cardiovascular protection[J]. Cardiovasc Drugs Ther,2017,31(1):77-86.

[29] Wang Y,Zhao R,Liu W,et al. Exosomal circHIPK3 Released from Hypoxia-Pretreated Cardiomyocytes Regulates Oxidative Damage in Cardiac Microvascular Endothelial Cells via the miR-29a/IGF-1 Pathway[J]. Oxid Med Cell Longev,2019,2019:7954657.

[30] Venkatesulu BP,Mahadevan LS,Aliru ML,et al. Radiation-induced endothelial vascular injury:a review of possible mechanisms[J]. JACC Basic Transl Sci,2018,3(4):563-572.

[31] Yentrapalli R,Azimzadeh O,Sriharshan A,et al. The PI3K/Akt/mTOR pathway is implicated in the premature senescence of primary human endothelial cells exposed to chronic radiation[J]. PloS one,2013,8(8):e70024.

[32] Dong X,Tong F,Qian C,et al. NEMO modulates radiation-induced endothelial senescence of human umbilical veins through NF-κB signal pathway[J]. Radiat Res,2015,183(1):82-93.

[33] Philipp J,Azimzadeh O,Subramanian V,et al. Radiation-induced endothelial inflammation is transferred via the secretome to recipient cells in a STAT-Mediated Process[J]. J Proteom Res,2017,16(10):3903-3916.

[34] Heo JI,Kim KI,Woo SK,et al. Stromal cell-derived factor 1 protects brain vascular endothelial cells from radiation-induced brain damage[J]. Cells,2019,8(10):1230.

[35] Stewart FA,Heeneman S,Te Poele J,et al. Ionizing radiation accelerates the development of atherosclerotic lesions in ApoE?/? mice and predisposes to an inflammatory plaque phenotype prone to hemorrhage [J].Am J Pathol,2006,168(2):649-658.

[36] Jang H,Kwak SY,Park S,et al. Pravastatin alleviates radiation proctitis by regulating thrombomodulin in irradiated endothelial cells[J]. Int J Mol Sci,2020,21(5):1897.

[37] Wu R,Zeng Y. Does angiotensin Ⅱ–aldosterone have a role in radiation-induced heart disease?[J]. Med Hypotheses,2009,72(3):263-266.

[38] Ferreira-Machado SC,Rocha NDN,Mencalha AL,et al. Up-regulation of angiotensin-converting enzyme and angiotensin Ⅱ type 1 receptor in irradiated rats[J]. Int J Radiat Biol,2010,86(10):880-887.

[39] Korystova A,Kublik L,Levitman MK,et al. Ionizing radiation enhances activity of angiotensin-converting enzyme in rat aorta[J]. Bull Exp Biol Med,2018,165(2):216-219.

[40] Kim YA,Korystova AF,Kublik LN,et al. Flavonoids decrease the radiation-induced increase in the activity of the angiotensin-converting enzyme in rat aorta[J]. Eur J Pharmacol,2018,837:33-37.

更新日期/Last Update: 2021-06-09