_1690100844 20230723082724000 Rovedar Daryoushbabazadeh@gmail.com Rovedar Research in Biotechnology and Environmental Science Res. Biotechnol. Environ. Sci. 2980-7743 06 16 2023 2 2 Hanieh Kazemnian Hassan Mehrad-Majd https://orcid.org/0000-0002-8745-6558 The current study aimed to overview recent advances in preventing and treating chemotherapy-induced cardiotoxicity. Chemotherapy is widely used in cancer treatment, however, it can have adverse effects on the heart, leading to the development of risk factors, such as hypertension, obesity, dyslipidemia, and metabolic syndrome. Anthracycline compounds are the most commonly used chemotherapy agents and are associated with an increased risk of developing anthracycline-induced cardiotoxicity (AIC). The precise mechanisms underlying AIC remain a subject of debate, but evidence suggests that the primary causes are the generation of reactive oxygen species (ROS) and subsequent oxidative stress. Several risk factors have been linked to the development of AIC, including cumulative dose, pre-existing cardiac disease, age, gender, and cardiac risk factors. Genetic susceptibility may also play a role as a potential risk factor for AIC. In order to protect cardiac function, various strategies have been explored, such as developing less-toxic derivatives of anthracyclines, determining safer cumulative anthracycline doses, and identifying new cardioprotective agents. Prophylactic treatment with cardioprotective agents is the best approach for high-risk patients. This article reviewed the present strategies for protecting cancer patients from AIC based on effective cardioprotective drugs along with the balance between their benefits and potential adverse effects. 06 16 2023 24 29 https://creativecommons.org/licenses/by/4.0 10.58803/rbes.v2i2.14 https://rbes.rovedar.com/index.php/RBES/article/view/14 https://rbes.rovedar.com/index.php/RBES/article/download/14/31 https://rbes.rovedar.com/index.php/RBES/article/download/14/31 10.1053/j.seminoncol.2013.01.008 10.1161/CIRCRESAHA.113.300218 10.1093/eurjhf/hfq213 10.1186/1471-2407-10-337 Cardinale D, Colombo A, Lamantia G, Colombo N, Civelli M, De Giacomi G, et al. Anthracycline-induced cardiomyopathy: Clinical relevance and response to pharmacologic therapy. J Am Coll Cardiol. 2010; 55(3): 213-220. DOI: 10.1016/j.jacc.2009.03.095 10.1016/S0006-2952(98)00307-4 10.1161/CIRCULATIONAHA.113.003688 Kocik M, Zimovjanova M, Petruzelka L, Kodydkova J, Vavrova L, and Zak A. Oxidative stress after anthracycline therapy in patients with solid tumors. Cas Lek Ces. 2012; 151(10): 463-467. Available at: https://pubmed.ncbi.nlm.nih.gov/23256630/ 10.4048/jbc.2013.16.2.178 10.1016/j.jacc.2014.06.1167 Unverferth DV, Magorien RD, Unverferth BP, Talley RL, Balcerzak SP, and Baba N. Human myocardial morphologic and functional changes in the first 24 hours after doxorubicin administration. Cancer Treat Rep. 1981; 65(11-12): 1093-1097. PubMed PMID: 7296554 10.1007/s11906-010-0146-y 10.1006/mgme.2000.3043 10.1016/j.yjmcc.2006.06.009 10.1161/01.RES.83.5.516 Childs AC, Phaneuf SL, Dirks AJ, Phillips T, and Leeuwenburgh C. Doxorubicin treatment in vivo causes cytochrome C release and cardiomyocyte apoptosis, as well as increased mitochondrial efficiency, superoxide dismutase activity, and Bcl-2: Bax ratio. Cancer Res. 2002; 62(16): 4592-4598. 10.2174/157340311799960645 10.1124/pr.56.2.6 10.1152/ajpheart.00407.2008 10.1126/science.6093249 10.1038/clpt.2013.201 10.1007/s00210-006-0091-0 10.1038/nm.2919 10.1002/1097-0142(19850615)55:12<2761::AID-CNCR2820551206>3.0.CO;2-P -2765. DOI: 10.1002/1097-0142(19850615)55:12%3C2761::AID-CNCR2820551206%3E3.0.CO;2-P Yeh ET, and Bickford CL. Cardiovascular complications of cancer therapy: Incidence, pathogenesis, diagnosis, and management. 10.1016/j.jacc.2009.02.050 10.1007/s10549-006-9413-7 10.7326/0003-4819-91-5-710 10.1200/JCO.2010.34.3467 10.2217/pgs.15.162 10.2217/pgs.15.61 Reichwagen A, Ziepert M, Kreuz M, Godtel-Armbrust U, Rixecker T, Poeschel V, et al. Association of NADPH oxidase polymorphisms with anthracycline-induced cardiotoxicity in the RICOVER-60 trial 10.2217/pgs.14.179 10.1200/JCO.2015.63.4550 10.1038/s41598-017-00075-1 10.1007/BF00257439 10.7326/0003-4819-96-2-133 10.2165/00002018-200124120-00004 10.1016/j.amjcard.2011.01.006 10.1067/mhj.2001.115436 10.1159/000046508 10.1373/clinchem.2005.050153 10.1002/cncr.11407 10.1161/CIR.0b013e3182a88099 10.1161/CIRCULATIONAHA.106.635144 10.1007/s00432-003-0498-7 10.1200/JCO.2005.02.3879 10.1634/theoncologist.10-6-427 10.1002/14651858.CD005008.pub3 10.31557/APJCP.2021.22.9.2847 10.1016/j.jacc.2018.02.049 10.1093/eurheartj/ehw022 10.1080/17512433.2019.1637252 10.1016/j.jacc.2006.07.052 10.1016/j.jacc.2009.03.095 10.1016/j.jacc.2012.07.067 DjoussÚ L, Akinkuolie AO, Wu JH, Ding EL, Gaziano JM. Fish consumption, omega-3 fatty acids and risk of heart failure: a 10.1016/j.clnu.2012.05.010 10.3389/fnut.2022.809311