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. 2020 Oct 13;2020:4894625. doi: 10.1155/2020/4894625

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Copyright © 2020 Xinyu Yang et al.

This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Mechanism of cardiotoxicity induced by susceptibility genes in chemotherapy. ROS: reactive oxygen species; NOX: nicotinamide adenine dinucleotide phosphate oxidase; POR: P450 oxidoreductase; GST: glutathione S-transferase; CYP3A5: cytochrome P450 family 3 subfamily A member 5; CAT: catalase; HAS3: hyaluronan synthase 3; SOD: superoxide dismutase; UVRAG: ultraviolet irradiation resistance-associated gene; GCN2: general control nonderepressible 2; eIF2α: eukaryotic initiation factor 2α; UCP2: uncoupling protein 2; Bcl-2: B-cell lymphoma-2; TCL1A: T cell leukemia/lymphoma 1A; HLA: human leukocyte antigen; TLR2: Toll-like receptor 2; TLR4: Toll-like receptor 4; TLR9: Toll-like receptor 9; Hmox1: heme oxygenase-1; CBR: carbonyl reductase; CBR1: carbonyl reductase 1; CBR3: carbonyl reductase 3; TTNtv: titin-truncating variants; DNMT1: DNA methyltransferase 1; GPR35: G protein-coupled receptor 35; HNMT: histamine n-ethyltransferase; RAS-related genes: renin-angiotensin system-related genes.