[1]Vejpongsa P, Yeh ET. Prevention of anthracycline-induced cardiotoxicity: challenges and opportunities.J Am Coll Cardiol. 2014,64(9):938-945. https://doi.org/10.1016/j.jacc.2014.06.1167
[2]Caron J, Nohria A.Cardiac Toxicity from Breast Cancer Treatment: Can We Avoid This?.Curr Oncol Rep. 2018,20(8):61. https://doi.org/10.1007/s11912-018-0710-1.
[3]Ye J,Fang L, Zheng H,et al. WEGO a web tool for plotting GO annotations.Nucleic Acids Res. 2006,34(Web Server issue):W293-297. https://doi.org/10.1093/nar/gkl031
[4] D. Cappetta, A. De Angelis, L. Sapio, et al., 2017.Oxidative stress and cellular response to doxorubicin: a common factor in the complex milieu of anthracycline cardiotoxicity. Oxid. Med. Cell Longev. 2017, 1521020. https://doi.org/10.1155/2017/1521020.
[5] R.W. Loar, C.V. Noel, H. Tunuguntla, et al., State of the art review: chemotherapy-induced cardiotoxicity in children, Congenit. Heart Dis. 13 (2017) 5–15. https://doi.org/10.1111/chd.12564.
[6] T. Simunek, M. Stérba, O. Popelov, et al., Anthracycline-induced cardiotoxicity: overview of studies examining the roles of oxidative stress and free cellular iron, Pharmacol. Rep.61 (2009) 154–171. https://doi.org/10.1016/S1734-1140(09)70018-0.
[7] X. Xu, H.L. Persson, D.R. Richardson, Molecular pharmacology of the interaction of anthracyclines with iron, Mol. Pharmacol. 68 (2005) 261–271. https://doi.org/10.1124/mol.105.013383.
[8] E. Barry, J.A. Alvarez, R.E. Scully, et al., Anthracycline-induced cardiotoxicity: course, pathophysiology, prevention and management, Expert Opin. Pharmacother. 8 (2007) 1039–1058. https://doi.org/10.1517/14656566.8.8.1039.
[9] S.L. Leong, N. Chaiyakunapruk, S.W. Lee, Candidate gene association studies of anthracycline-induced cardiotoxicity: a systematic review and meta-analysis, Sci Rep. 7 (2017) 39. https://doi.org/10.1038/s41598-017-00075-1.
[10] K.B. Wallace, Doxorubicin-induced cardiac mitochondrionopathy, Pharmacol. Toxicol. 93 (2003) 105–115. https://doi.org/10.1034/j.1600-0773.2003.930301.x.
[11] D. Lebrecht, U.A. Walker, Role of mtDNA lesions in anthracycline cardiotoxicity, Cardiovasc. Toxicol. 7 (2007) 108–113. https://doi.org/10.1007/s12012-007-0009-1.
[12] D. Lebrecht, A. Kokkori, U.P. Ketelsen, et al., Tissue-specific mtDNA lesions and radical-associated mitochondrial dysfunction in human hearts exposed to doxorubicin, J.Pathol. 207 (2005) 436–444. https://doi.org/10.1002/path.1863.
[13] P.A. Jones, J.P. Issa, S. Baylin, Targeting the cancer epigenome for therapy, Nat. Rev. Genet. 17 (2016) 630–641. https://doi.org/10.1038/nrg.2016.93.
[14] T.E. Callis, Wang DZ, Taking microRNAs to heart, Trends Mol. Med. 14 (2008) 254–260. https://doi.org/10.1016/j.molmed.2008.03.006.
[15] G.B. Fogel, Z.S. Kai, S. Zargar, et al., MicroRNA dynamics during human embryonic stem cell differentiation to pancreatic endoderm, Gene. 574 (2015) 359–370. https://doi.org/10.1016/j.gene.2015.08.027.
[16] J.N. Zhu, Y.H. Fu, Z.Q. Hu, et al., 2017. Activation of miR-34a-5p/Sirt1/p66shc pathway contributes to doxorubicin-induced cardiotoxicity. Sci. Rep. 7, 11879. https://doi.org/10.1038/s41598-017-12192-y.
[17] D. Terentyev, A.E. Belevych, R. Terentyeva, et al., miR21 overexpression enhances Ca2+ release and promotes cardiac arrhythmogenesis by targeting PP2A regulatory subunitB56 and causing caMKⅡ-dependent hyperphosphorylation of RyR2, Circ. Res. 104 (2009) 514–521. https://doi.org/10.1161/CIRCRESAHA.108.181651.
[18] W.J. Wijnen, Y.M. Pinto, E.E. Creemers., 2013. The therapeutic potential of miRNAs in cardiac fibrosis: where do we stand? J Cardiovasc. Transl. Res. 6 (6) 899–908. https://doi.org/10.1007/s12265-013-9483-y.
[19]Ishikawa H, Ide T, Yagi T,et al.TTC26/DYF13 is an intraflagellar transport protein required for transport of motility-related proteins into flagella. Elife. 2014 ,3:e02897. doi: 10.7554/eLife.02897.
[20]Pérez-Victoria FJ, Mardones GA, Bonifacino JS.Requirement of the human GARP complex for mannose 6-phosphate-receptor-dependent sorting of cathepsin D to lysosomes. Mol Biol Cell. 2008 ,19(6):2350-62. doi: 10.1091/mbc.E07-11-1189.
[21]Wei J, Zhang YY, Luo J.et al.The GARP Complex Is Involved in Intracellular Cholesterol Transport via Targeting NPC2 to Lysosomes.Cell Rep. 2017,27;19(13):2823-2835.
doi: 10.1016/j.celrep.2017.06.012
[22]Shimokawa H, Rashid M. Development of Rho kinase inhibitors for cardiovascular medicine.Trends Pharmacol Sci. 2007,28(6):296-302.doi: 10.1016/j.tips.2007.04.006
[23]Surma M, Wei L, Shi J.Rho kinase as a therapeutic target in cardiovascular disease.Future Cardiol. 2011,7(5):657-71.doi: 10.2217/fca.11.51
[24]Sysa-Shah P, Xu Y, Guo X, Pin S, Bedja D, Bartock R, Tsao A, Hsieh A, Wolin MS, Moens A, Raman V, Orita H, Gabrielson KL.Geranylgeranylacetone blocks doxorubicin-induced cardiac toxicity and reduces cancer cell growth and invasion through RHO pathway inhibition. Mol Cancer Ther. 2014,13(7):1717-728. doi: 10.1158/1535-7163.
[25]Shi J, Surma M, Wei L. Disruption of ROCK1 gene restores autophagic flux and mitigates doxorubicin-induced cardiotoxicity. Oncotarget. 2018,9(16):12995-13008. doi:10.18632/oncotarget.24457.
[26]Huang CY, Chen JY, Kuo CH, Pai PY, Ho TJ, Chen TS, Tsai FJ, Padma VV, Kuo WW, Huang CY.Mitochondrial ROS-induced ERK1/2 activation and HSF2-mediated AT1 R upregulation are required for doxorubicin-induced cardiotoxicity. J Cell Physiol. 2018,233(1):463-475. doi:10.1002/jcp.25905.
[27]Yang L, Luo C, Chen C, Wang X, Shi W, Liu J.All-trans retinoic acid protects against doxorubicin-induced cardiotoxicity by activating the ERK2 signalling pathway. Br J Pharmacol. 2016,173(2):357-71.doi:10.1111/bph.13377.
[28]Eldridge S, Guo L, Mussio J, Furniss M, Hamre J 3rd, Davis M.Examining the protective role of ErbB2 modulation in human-induced pluripotent stem cell-derived cardiomyocytes.Toxicol Sci. 2014,141(2):547-59. doi:10.1093/toxsci/kfu150.