[1]王鹏 王鑫 张瑶 张经泽 贺世豪 李瑾.内质网应激在阿霉素心脏毒性中作用的研究进展[J].心血管病学进展,2023,(4):341.[doi:10.16806/j.cnki.issn.1004-3934.2023.04.012]
 WANG Peng,WANG Xin,ZHANG Yao,et al.Role of Endoplasmic Reticulum Stress?n the Cardiotoxicity of Doxorubicin[J].Advances in Cardiovascular Diseases,2023,(4):341.[doi:10.16806/j.cnki.issn.1004-3934.2023.04.012]
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内质网应激在阿霉素心脏毒性中作用的研究进展()
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《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2023年4期
页码:
341
栏目:
综述
出版日期:
2023-04-25

文章信息/Info

Title:
Role of Endoplasmic Reticulum Stress?n the Cardiotoxicity of Doxorubicin
作者:
王鹏1 王鑫1 张瑶1 张经泽 1 贺世豪1 李瑾2
(1.山西医科大学第二临床医学院,山西 太原 030000;2.山西医科大学第二医院心血管内科,山西 太原 030000)
Author(s):
WANG Peng1 WANG Xin1 ZHANG Yao1 ZHANG Jingze1 HE Shihao1 LI Jin2
?1.The Second Clinical Medical College of Shanxi Medical UniversityTaiyuan 030000ShanxiChina2.Department of CardiologyThe Second Hospital of Shanxi Medical UniversityTaiyuan 030000ShanxiChina)
关键词:
内质网应激未折叠蛋白反应阿霉素心脏毒性
Keywords:
Endoplasmic reticulum stressUnfolded protein responseDoxorubicinCardiotoxicity
DOI:
10.16806/j.cnki.issn.1004-3934.2023.04.012
摘要:
阿霉素作为抗肿瘤药,疗效确切,应用广泛,但其具有显著的心脏毒性。细胞受到各种刺激时,内质网内错误折叠蛋白及未折叠蛋白蓄积,产生内质网应激,继而触发未折叠蛋白反应,以恢复细胞内蛋白稳态,但持续激活的未折叠蛋白反应会诱发细胞凋亡。目前认为持续激活的未折叠蛋白反应所致心肌细胞凋亡与阿霉素心脏毒性有关,且许多化合物及药物可能通过抑制内质网应激发挥阿霉素心脏毒性保护作用。现对阿霉素心脏毒性中内质网应激及其所致凋亡以及可能以该途径为靶点保护的化合物及药物进行综述。
Abstract:
As an antitumor drug,doxorubicin is effective and widely used ,but it has significant cardiotoxicity. When cells are subjected to various stimuli,intracellular misfolded or unfolded proteins accumulate,resulting in endoplasmic reticulum stress,which triggers unfolded protein responses to restore intracellular protein homeostasis,but persistently activated unfolded protein responses can induce apoptosis. It is currently believed that cardiomyocyte apoptosis caused by the continuously activated unfolded protein response is related to the cardiotoxicity of doxorubicin,and many compounds and drugs may play a protective effect on the cardiotoxicity of doxorubicin by inhibiting endoplasmic reticulum stress. This article reviews endoplasmic reticulum stress and apoptosis by endoplasmic reticulum stress in doxorubicin-induced cardiotoxicity ,as well as protective compounds and drugs that may target this pathway

参考文献/References:

[1] Hetz C,Zhang K,Kaufman RJ. Mechanisms,regulation and functions of the unfolded protein response[J]. Nat Rev Mol Cell Biol,2020,21(8):421-438.

[2] Guo Y,Guo R,Su Y,et al. The PERK/eIF2α/ATF4/CHOP pathway plays a role in regulating monocrotaline-induced endoplasmic reticulum stress in rat liver[J]. Res Vet Sci,2020,130:237-239.

[3] Bagchi AK,Malik A,Akolkar G,et al. Study of ER stress and apoptotic proteins in the heart and tumor exposed to doxorubicin[J]. Biochim Biophys Acta Mol Cell Res,2021,1868(7):119039.

[4] Tsaytler P,Harding HP,Ron D,et al. Selective inhibition of a regulatory subunit of protein phosphatase 1 restores proteostasis[J]. Science,2011,332(6025):91-94.

[5] Hu H,Tian M,Ding C,et al. The C/EBP homologous protein (CHOP) transcription factor functions in endoplasmic reticulum stress-induced apoptosis and microbial infection[J]. Front Immunol,2019,9:3083.

[6] Kuang H,Yang P,Yang L,et al. Size dependent effect of ZnO nanoparticles on endoplasmic reticulum stress signaling pathway in murine liver[J]. J Hazard Mater,2016,317:119-126.

[7] Nishida T,Hattori K,Watanabe K. The regulatory and signaling mechanisms of the ASK family[J]. Adv Biol Regul,2017,66:2-22.

[8] Yue J,López JM. Understanding MAPK signaling pathways in apoptosis[J]. Int J Mol Sci,2020,21(7):2346.

[9] Karna KK,Shin YS,Choi BR,et al. The role of endoplasmic reticulum stress response in male reproductive physiology and pathology:a review[J]. World J Mens Health,2020,38(4):484-494.

[10] Fu HY,Sanada S,Matsuzaki T,et al. Chemical endoplasmic reticulum chaperone alleviates doxorubicin-induced cardiac dysfunction[J]. Circ Res,2016,118(5):798-809.

[11] Malik A,Bagchi AK,Jassal DS,et al. Interleukin-10 mitigates doxorubicin-induced endoplasmic reticulum stress as well as cardiomyopathy[J]. Biomedicines,2022,10(4):890.

[12] Wang M,Zhang J,Zhao M,et al. Resolvin D1 attenuates doxorubicin-induced cardiotoxicity by inhibiting inflammation,oxidative and endoplasmic reticulum stress[J]. Front Pharmacol,2022,12:749899.

[13] Dhanasekaran DN,Reddy EP. JNK-signaling:a multiplexing hub in programmed cell death[J]. Genes Cancer,2017,8(9-10):682-694.

[14] Grynberg K,Ma FY,Nikolic-Paterson DJ. The JNK signaling pathway in renal fibrosis[J]. Front Physiol,2017,8:829.

[15] Aubrey BJ,Kelly GL,Janic A,et al. How does p53 induce apoptosis and how does this relate to p53-mediated tumour suppression?[J]. Cell Death Differ,2018,25(1):104-113.

[16] Hang P,Zhao J,Sun L,et al. Brain-derived neurotrophic factor attenuates doxorubicin-induced cardiac dysfunction through activating Akt signalling in rats[J]. J Cell Mol Med,2017,21(4):685-696.

[17] Meijles DN,Cull JJ,Markou T,et al. Redox regulation of cardiac ASK1 (apoptosis signal-regulating kinase 1) controls p38-MAPK (mitogen-activated protein kinase) and orchestrates cardiac remodeling to hypertension[J]. Hypertension,2020,76(4):1208-1218.

[18] Lou Y,Wang Z,Xu Y,et al. Resveratrol prevents doxorubicin-induced cardiotoxicity in H9c2 cells through the inhibition of endoplasmic reticulum stress and the activation of the Sirt1 pathway[J]. Int J Mol Med,2015,36(3):873-880.

[19] Gal R,Deres L,Toth K,et al. The effect of resveratrol on the cardiovascular system from molecular mechanisms to clinical results[J]. Int J Mol Sci,2021,22(18):10152.

[20] Zhang L,Chen J,Yan L,et al. Resveratrol ameliorates cardiac remodeling in a murine model of heart failure with preserved ejection fraction[J]. Front Pharmacol,2021,12:646240.

[21] Restini CBA,Garcia AFE,Natalin HM,et al. Resveratrol supplants captopril’s protective effect on cardiac remodeling in a hypertension model elicited by renal artery stenosis[J]. Yale J Biol Med,2022,95(1):57-69.

[22] Monahan DS,Flaherty E,Hameed A,et al. Resveratrol significantly improves cell survival in comparison to dexrazoxane and carvedilol in a h9c2 model of doxorubicin induced cardiotoxicity[J]. Biomed Pharmacother,2021,140:111702.

[23] 李红艳,宋洪强. 新型促炎消退介质——消退素的生物效应及机制[J]. 中国老年学杂志,2020,40(11):2451-2454.

[24] Jung TW,Hwang HJ,Hong HC,et al. Resolvin D1 reduces ER stress-induced apoptosis and triglyceride accumulation through JNK pathway in HepG2 cells[J]. Mol Cell Endocrino,2014,391(1-2):30-40.

[25] Zhang J,Wang M,Ding W,et al. Resolvin E1 protects against doxorubicin-induced cardiotoxicity by inhibiting oxidative stress,autophagy and apoptosis by targeting AKT/mTOR signaling[J]. Biochem Pharmacol,2020,180:114188.

[26] Xu S,Zhang J,Liu J,et al. The role of interleukin-10 family members in cardiovascular diseases[J]. Int Immunopharmacol,2021,94:107475.

[27] Gao L,Yuan P,Wei Y,et al. Total flavonoids of Selaginella tamariscina (P.Beauv.) Spring ameliorates doxorubicin-induced cardiotoxicity by modulating mitochondrial dysfunction and endoplasmic reticulum stress via activating MFN2/PERK[J]. Phytomedicine,2022,100:154065.

[28] Xu ZM,Li CB,Liu QL,et al. Ginsenoside Rg1 prevents doxorubicin-induced cardiotoxicity through the inhibition of autophagy and endoplasmic reticulum stress in mice[J]. Int J Mol Sci,2018,19(11):3658.

[29] Zhang Y,Kong D,Han H,et al. Caffeic acid phenethyl ester protects against doxorubicin-induced cardiotoxicity and increases chemotherapeutic efficacy by regulating the unfolded protein response[J]. Food Chem Toxicol,2022,159:112770.

[30] Rawat PS,Jaiswal A,Khurana A,et al. Doxorubicin-induced cardiotoxicity:an update on the molecular mechanism and novel therapeutic strategies for effective management[J]. Biomed Pharmacother,2021,139:111708.

[31] Martín‐Garcia A,López‐Fernández T,Mitroi C,et al. Effectiveness of sacubitril-valsartan in cancer patients with heart failure[J]. ESC Heart Failure,2020,7(2):763-767.

[32] Kim BS,Park IH,Lee AH,et al. Sacubitril/valsartan reduces endoplasmic reticulum stress in a rat model of doxorubicin-induced cardiotoxicity[J]. Arch Toxicol,2022,96(4):1065-1074.

[33] Chang WT,Lin YW,Ho CH,et al. Dapagliflozin suppresses ER stress and protects doxorubicin-induced cardiotoxicity in breast cancer patients[J]. Arch Toxicol,2021,95(2):659-671.

[34] 吴锦波,叶小汉,冼绍祥,等. 比索洛尔联合培哚普利对阿霉素诱导的心力衰竭大鼠心肌内质网应激的影响[J]. 中国病理生理杂志,2016,32(11):1939-1944.

[35] 贺智慧,邵立群,宣丽颖,等. 黄芪注射液对阿霉素性心肌细胞凋亡、内质网应激与缝隙连接蛋白表达的影响[J]. 中国应用生理学杂志,2018,34(2):159-163.

[36] 马奎影,万全,王伊林,等. 黄芪注射液对网腔钙结合蛋白基因沉默阿霉素损伤心肌细胞内质网应激伴侣蛋白GRP78,GRP94 mRNA的作用[J]. 中国应用生理学杂志,2016,32(2):154-157.

[37] 刘福,李欣. 富参颗粒对阿霉素诱导心力衰竭大鼠心肌细胞凋亡及内质网应激相关蛋白表达的影响[J]. 中国医师杂志,2017,19(4):556-559.

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更新日期/Last Update: 2023-05-17