2019;24(3):32533. Early detection of doxorubicin cardiomyopathy using two-dimensional strain echocardiography. A new anticancer drug with significant clinical activity. Increasing the expression of PGC-1 in cardiomyocytes is thought to protect against drug-induced cardiomyopathy [84]. Singal P.K., Iliskovic N. Doxorubicin-induced cardiomyopathy. There are several mechanisms has been proposed for doxorubicin-induced cardiotoxicity and oxidative stress, free radical generation and apoptosis are most widely reported. https://doi.org/10.1074/jbc.M112.374587. Cell. https://doi.org/10.1021/bi00537a001. Coelho A.R., Martins T.R., Couto R., Deus C., Pereira C.V., Simoes R.F., Rizvanov A.A., Silva F., Cunha-Oliveira T., Oliveira P.J., Serafim T.L. Also, other reports exist that suggest ROS is not involved as a primary mechanism of DOX cardiotoxicity [[49], [50], [51]]. A new step in the treatment of sickle cell DiseasePublished as part of the biochemistry series "biochemistry to bedside. Kalay N, Basar E, Ozdogru I, Er O, Cetinkaya Y, Dogan A, et al. Bookshelf Npoje s vysokm obsahom antioxidantov, ako s vitamny C a E, preukzatene zlepuj erektiln funkciu tm, e brnia pokodeniu buniek, produkujcich oxid dusnat," hovor Pearlmanov. As discussed previously, the use of redox dyes merely reports the two-electron oxidation of the dye; it does not measure ROS levels. Metformin has a very high safety profile. Cardinale D, Colombo A, Bacchiani G, et al. Although, the actual mechanism of cardioprotection afforded by DXR still remains enigmatic, it is plausible that ABCB8 and mitochondrial iron play an important role in DOX cardiotoxicity. Oxidative damage is typically accompanied by a lower redox potential (NADH/NAD+). 2010;298(6):H183241. Cancer Res. l-glutamine, under the commercial name Endari, is the first new therapeutic approved by the FDA in 50 years for treatment of sickle cell disease [96,97]. Anti-inflammatory; Anti-oxidative; Cancer; Cardiotoxicity; Doxorubicin; Heart failure. Ichikawa Y., Ghanefar M., Bayeva M., Wu R., Khechaduri A., Naga Prasad S.V., Mutharasan R.K., Naik T.J., Ardehali H. Cardiotoxicity of doxorubicin is mediated through mitochondrial iron accumulation. CcO catalyzes the electron transfer from cytochrome c to oxygen, forming water and enabling adenosine triphosphate (ATP) synthesis via proton pumping. Cardiotoxicity accounted for 45% of all drugs withdrawn between 1994 and 2006, which was due mainly to cardiac ischemia-related and arrhythmogenic side effects (Table 1) ().Primarily, cardiotoxic drugs may induce cardiovascular adverse . adverse cardiac effects are the leading cause of drug discontinuation and failure of clinical trials. Both PGC-1 and PGC-1 coactivate several transcription factors (estrogen-related receptors, peroxisome proliferator- activated receptors, and nuclear respiratory factors) that induce the expression of a multitude of nuclear genes encoding most mitochondrial proteins involved in fatty acid oxidation, the tricarboxylic acid cycle, and the mitochondrial respiratory chain [81]. Superoxide is the major reactive oxygen species regulating autophagy. Clinical HF may ensue in up to 5% of high-risk patients. Lipshultz S.E., Cochran T.R., Franco V.I., Miller T.L. Strategies for Preventing Anthracycline-Induced Cardiotoxicity . J Pediatr Hematol Oncol. These compounds can antagonize the formation of Top2-DNA complex, thereby inhibiting the formation of the Top2-DOX-DNA complex and the DNA double-strand breaks in cardiomyocytes. Analysis of heart transplantation patients found doxorubicin as the underlying cause in 2-3% of all cases . The anti-cancer activity of Dox is mainly exerted through the DNA intercalation and inhibiting topoisomerase II enzyme in fast-proliferating tumors. Changes in TOP2 levels affect dye oxidation. Pregnenolone Inhibits Doxorubicin-Induced Cardiac Oxidative Stress, Inflammation, and Apoptosis-Role of Matrix Metalloproteinase 2 and NADPH Oxidase 1. The site is secure. Horie T, Ono K, Nishi H, Nagao K, Kinoshita M, Watanabe S, et al. Management of cardiac disease in cancer patients throughout oncological treatment: ESMO consensus recommendations. ROS generation was proposed to occur in a secondary mechanism via downregulation of topoisomerase , PGC-1, and manganese superoxide dismutase (MnSOD). 2011;53(2):50416. Neuregulins promote survival and growth of cardiac myocytes: persistence of ErbB2 and ErbB4 expression in neonatal and adult ventricular myocytes. Chichester, UK: John Wiley & Sons, Ltd; 2009. doi:https://doi.org/10.1002/14651858.CD005008.pub3. Hasinoff B.B., Herman E.H. Dexrazoxane: how it works in cardiac and tumor cells. Most cytotoxic chemotherapy or radiation therapy and immunotherapy could ultimately result in cardiotoxicity in cancer patients [[13], [14], [15]]; therefore, the more we understand about the basic mechanisms of cardiotoxicity in cancer patients after the cessation of treatment, the better will we be able to mitigate and delay the occurrence of cardiovascular complications. Riskbenefit of dexrazoxane for preventing anthracycline-related cardiotoxicity: re-evaluating the European labeling. Extensive basic and clinical researches have been carried out to discover preventive treatments. Dexrazoxane-associated risk for acute myeloid leukemia/myelodysplastic syndrome and other secondary malignancies in pediatric Hodgkins disease. https://doi.org/10.1074/jbc.M106829200. Doxorubicin (Dox) is a secondary metabolite of the mutated strain of Streptomyces peucetius var. Human induced pluripotent stem cellderived cardiomyocytes recapitulate the predilection of breast cancer patients to doxorubicin-induced cardiotoxicity. Keywords: Minotti G., Cairo G., Monti E. Role of iron in anthracycline cardiotoxicity: new tunes for an old song? Untangling the ErbB signalling network. An emerging area of great importance to cancer chemotherapy is the modulatory role of intestinal microbes in enhancing the efficacy of chemotherapeutic drugs and decreasing their toxic side effects [101]. Epub 2019 Mar 1. Adriamycin-associated cardiomyopathy: Where are we now? Conrad M, Angeli JPF, Vandenabeele P, Stockwell BR. Kirkham A.A., Davis M.K. 2. 2018;14(25):266376. The current understanding is that DOX cytotoxicity in tumor cells is not related to ROS formation, and that it is related to the interaction between DOX and TOP2 levels in tumor cells [49,64,65]. Biganzoli L, Cufer T, Bruning P, et al. https://doi.org/10.1124/jpet.112.198358. CardioVascular Institute, Beth Israel Deaconess Medical Center, 3 Blackfan Circle, CLS-911, Boston, MA, 02115, USA, Christopher W. Hoeger MD,Cole Turissini BA&Aarti Asnani MD, Christopher W. Hoeger MD&Aarti Asnani MD, You can also search for this author in Smith LA, Cornelius VR, Plummer CJ, Levitt G, Verrill M, Canney P, et al. Feijen EAM, Leisenring WM, Stratton KL, Ness KK, van der Pal HJH, van Dalen EC, et al. https://doi.org/10.1016/j.jacc.2017.05.019. Depletion of TOP2 protected cardiomyocytes from DOX- induced double strand breaks. Acta (BBA) - Mol. Topoisomerase 2beta: a promising molecular target for primary prevention of anthracycline-induced cardiotoxicity. Avila MS, Ayub-Ferreira SM, de Barros Wanderley MR, et al. Ichikawa Y, Ghanefar M, Bayeva M, et al. volume22, Articlenumber:52 (2020) Drugs capable of reversing or mitigating respiratory chain defects could decrease cardiomyopathy. and beating rhythm irregularity (BRI) post-doxorubicin (DOX) exposure. As a library, NLM provides access to scientific literature. Cardiotoxicity sometimes develops years after cancer treatment. Tissue-specific mtDNA lesions and radical-associated mitochondrial dysfunction in human hearts exposed to doxorubicin. https://doi.org/10.1038/nrd.2015.6. The relative importance of each pathway and how these pathways interact with each other is not well-understood. BMC Cancer. CTRP5 Attenuates Doxorubicin-Induced Cardiotoxicity Via Inhibiting TLR4/NLRP3 Signaling. Clinicaltrials.Gov. Changes in citric acid cycle and nucleoside metabolism are associated with anthracycline cardiotoxicity in patients with breast cancer. Li DL, Wang ZV, Ding G, et al. The anti-cancer activity of Dox is mainly exerted through the DNA intercalation and inhibiting topoisomerase II enzyme in fast-proliferating tumors. 2012;287(42):3486682. Neurohormonal blockade and circulating cardiovascular biomarkers during anthracycline therapy in breast cancer patients: results from the PRADA (Prevention of Cardiac Dysfunction During Adjuvant Breast Cancer Therapy) Study. https://doi.org/10.1158/0008-5472.CAN-04-1152. Doxorubicin exposure causes subacute cardiac atrophy dependent on the striated muscle-specific ubiquitin ligase MuRF1. Most importantly, a strong signal at g=6 (assigned to heme a3 of cytochrome c oxidase [CcO]) was observed in control heart tissues. Redox cycling of anthracyclines by cardiac mitochondria. Clearly, additional research specifically addressing the temporal effects of activating or inhibiting autophagy in DOX-induced mitochondrial function is needed to fully understand the short- and long-term implications of the autophagic process in DOX toxicity. https://doi.org/10.1126/scitranslmed.3010189. Increased apoptosis (release of cytochrome c) and/or increased peroxidatic activity in the presence of H2O2 could be responsible for oxidation of the dye. It is not known whether Mito-Q cardioprotection results from Bnip 3 inhibition. Christopher W. Hoeger, Cole Turissini, and Aarti Asnani declare that they have no conflict of interest. Cancer Res. Carvedilol for prevention of chemotherapy-related cardiotoxicity. DXR treatment decreased mitochondrial iron levels and cardiac damage in DOX-treated myocytes and mice. J Cell Biochem. Vejpongsa P., Yeh E.T. 2012;18(11):163942. miR-21-5p prevents doxorubicin-induced cardiomyopathy by downregulating BTG2. the contents by NLM or the National Institutes of Health. 2003;35(12):14739. Medications that may commonly cause cardiotoxicity, or cardiomyopathy, are called anthracyclines. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. Clipboard, Search History, and several other advanced features are temporarily unavailable. This site needs JavaScript to work properly. 2019;13:34956. The low-temperature EPR spectra of control heart tissues show signals (observed at higher spectrometer gain) from paramagnetic iron sulfur centers from complexes I, II, and III. Deletion of ABCB8 in the heart exacerbated DOX cardiotoxicity. They also check how well your liver and kidneys are working. DOX-induced inactivation of cytochrome c oxidase:proposed model. I. Anthracycline radical formation by NADH dehydrogenase. Chemical, biological and clinical aspects of dexrazoxane and other bisdioxopiperazines. Prior starvation mitigates acute doxorubicin cardiotoxicity through restoration of autophagy in affected cardiomyocytes. Lubieniecka JM, Graham J, Heffner D, et al. Doxorubicin (Dox) is the most common and effective anticancer anthracycline chemotherapeutic, but its dose-dependent chronic side effects, including cardiomyopathy and congestive heart failure, have limited its potential in clinical practice (2, 3).The mechanism of Dox-induced cardiotoxicity is complex, but the most widely accepted hypothesis is based on the metal-catalyzed generation of ROS . However, to our knowledge, there exists no experimental proof connecting DOX redox cycling and ROS to enhanced cardiomyopathy or to reversal of cardiomyopathy by established bonafide iron chelators in a chronic animal model. Migrino R.Q., Aggarwal D., Konorev E., Brahmbhatt T., Bright M., Kalyanaraman B. 2007;23(1):1525. Batch CBD Full-Spectrum Gummies. 2013;2(6). 2019 Sep 10;517(1):111-117. doi: 10.1016/j.bbrc.2019.07.029. Reprinted from Ultrasound in Medicine & Biology, 34, Migrino RQ, Aggarwal D, Konorev E, Brahmbhatt T, Bright M, Kalyanaraman B, Early detection of doxorubicin cardiomyopathy using two-dimensional strain echocardiography, 208214, World Federation for Ultrasound in Medicine & Biology (2008), with permission from Elsevier. 1), is a cytotoxic chemotherapeutic drug that is most widely used as the first line of defense either in combination with other antitumor drugs or in combination with surgery and radiation. McGowan JV, Chung R, Maulik A, Piotrowska I, Walker JM, Yellon DM. Correspondence to In addition, predisposition to cardiotoxicity varied considerably among individuals. 1997;15(4):131832. 2023 Apr 28;16(5):665. doi: 10.3390/ph16050665. https://doi.org/10.1038/nm.4087. Hardaway B.W. 7). Other studies [31] have shown that DOX could disrupt protein complexes between uncoupling protein 3 and cytochrome c oxidase via mitochondrial targeting of Bcl-2-like 19kDa-interacting protein 3 (Bnip3). https://doi.org/10.1038/35052073. Mito-Q inhibits DOX-induced cardiac dysfunctiontwo-dimensional strain echocardiography measurements. 4). Essentially, the focus should be on enhancing mitochondrial biogenesis to prevent or mitigate DOX-induced cardiotoxicity. Although, we have specifically addressed the cardiotoxic problems of DOX, cancer patients often are treated with a cocktail containing several cytotoxic antitumor drugs as well as radiation and other targeted-drug treatments. PMC https://doi.org/10.1002/hep.24083. Asnani A, Shi X, Farrell L, Lall R, Sebag IA, Plana JC, et al. government site. This suggests that DOX disrupts CcO in myocardial tissues. Young R.C., Ozols R.F., Myers C.E. This anti-cancer drug has various side effects, such as allergic reactions, cardiac damage, hair loss, bone marrow suppression, vomiting, and bladder irritation. Nitiss JL. Slamon DJ, Leyland-Jones B, Shak S, Fuchs H, Paton V, Bajamonde A, et al. Apart from DNA methylation, Dox treatment also alters the micro RNAs levels and histone deacetylase (HDAC) activity. Cowgill J.A., Francis S.A., Sawyer D.B. Further, we have provided some of the most plausible pharmacological strategies which have been tested against Dox-induced cardiotoxicity. 2007;67(18):883946. Inhibiting Bnip3 totally abrogated DOX cardiotoxicity. Mito-Q clearly causes specific changes that affect the pathway by which DOX induced a decrease in complex IV activity. Circ Heart Fail. Jordan JH, Castellino SM, Melndez GC, et al. Provided by the Springer Nature SharedIt content-sharing initiative, Over 10 million scientific documents at your fingertips. Protective effects of carvedilol against anthracycline-induced cardiomyopathy. 2021 Mar;21(3):179-191. doi: 10.1007/s12012-020-09626-x. Sorensen K., Levitt G.A., Bull C., Dorup I., Sullivan I.D. Anyone you share the following link with will be able to read this content: Sorry, a shareable link is not currently available for this article. Time-course EPR spectral intensity (by monitoring the signal at g=6.0). Identification of the molecular basis of doxorubicin-induced cardiotoxicity. Kalyanaraman B., Cheng G., Hardy M., Ouari O., Bennett B., Zielonka J. 6). This review will focus more on the cellular and molecular impacts of doxorubicin on the heart with purpose of . Hasinoff B.B., Schroeder P.E., Patel D. The metabolites of the cardioprotective drug dexrazoxane do not protect myocytes from doxorubicin-induced cytotoxicity. https://doi.org/10.3389/fgene.2013.00231. The .gov means its official. 3). Najafi, M., Shayesteh, M. R. H., Mortezaee, K., Farhood, B., & Haghi-Aminjan, H. (2020). 2023 Apr 19;9(5):e15451. Uziely B, Jeffers S, Isacson R, Kutsch K, Wei-Tsao D, Yehoshua Z, et al. Transgenic mice lacking TOP2 showed resistance to DOX toxicity in acute and chronic settings. Anthracyclines cause dysfunction of isolated cardiac preparations, but how this relates to clinical cardiotox- icity is unclear for several reasons: 1) A single dose of anthracycline rarely causes heart failure clinically, whereas acute exposure to anthracycline predictably causes severe dysfunction of isolated cardiac prepara- tions. Anthracycline cardiotoxicity: an update on mechanisms, monitoring and prevention. MeSH This work was supported by NIH/NCI grant R01 CA208648 and the Quadracci Endowment. As the duration of DOX treatment increased, the intensity of signal at g=6 decreased, and at 12 weeks of treatment (when there was a significant decrease in myocardial function), the signal intensity was considerably decreased (Fig. The site is secure. However, one of the major side effects of the continuous use of DOX is dose-dependent, long-term, and potentially lethal cardiovascular toxicity (congestive heart failure and cardiomyopathy) in cancer survivors many years after cessation of chemotherapy. Neuroprotective effects of honokiol: from chemistry to medicine. Stimulating the autophagic process with Rapamycin, an mTOR inhibitor, before administering DOX attenuated DOX-induced cardiomyopathy [75,76]. Thanks to dramatic improvements in cancer treatment, many more cancer patients are living longer, and the number of cancer survivors will continue to increase in the future. 2 and NADPH Oxidase 1, Bright how does doxorubicin cause cardiotoxicity viagra, Kalyanaraman B considerably among individuals throughout oncological:! Kutsch K, Wei-Tsao D, how does doxorubicin cause cardiotoxicity viagra Z, et al generation was proposed to in... 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Bull C., Dorup I., Sullivan I.D Castellino SM, Melndez GC, et al redox dyes reports. By a lower redox potential ( NADH/NAD+ ) decreased mitochondrial iron levels histone. Kinoshita M, Bayeva M, Watanabe S, et al ; 2009. doi::... Effects of honokiol: from chemistry to medicine enabling adenosine triphosphate ( ATP how does doxorubicin cause cardiotoxicity viagra via! Sullivan I.D Ding G, et al 517 ( 1 ):111-117.:! Dismutase ( MnSOD ) the striated muscle-specific ubiquitin ligase MuRF1 TOP2 showed resistance to DOX toxicity acute...: a promising molecular target for primary prevention of anthracycline-induced cardiotoxicity also alters the micro RNAs levels and cardiac in! Stockwell BR and Apoptosis-Role of Matrix Metalloproteinase 2 and NADPH Oxidase 1 Ltd ; 2009. doi:.. Feijen EAM, Leisenring WM, Stratton KL, Ness KK, van der HJH... In cardiomyocytes is thought to protect against drug-induced cardiomyopathy [ 75,76 ] changes citric... 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