{"title":"Doxorubicin and cyclophosphamide mode of chemotherapy–related cardiomyopathy: Review of preclinical model","authors":"Ashot Avagimyan , Lev Kakturskiy , Nana Pogosova , Giulia Ottaviani , Manfredi Rizzo , Nizal Sarrafzadegan","doi":"10.1016/j.cpcardiol.2024.102882","DOIUrl":null,"url":null,"abstract":"<div><div>Over the past 70 years, there has been extensive research focused on preventing chemotherapy-related cardiovascular complications. However, the current state of cardio-oncology research has raised more questions than answers. Experimental studies often present data that are difficult to compare and, at times, contradictory. One notable limitation in translating experimental findings to clinical practice is the reliance on models that administer only one chemotherapeutic drug to experimental animals, despite the common use of multidrug cancer treatments in real clinical settings. This article aims to discuss our own experience in modeling an experimental rat model of cardiomyopathy induced by the administration of two chemotherapeutic drugs, doxorubicin (adriamycin) and cyclophosphamide (AC mode of chemotherapy) – Avagimyan A., et al model, along with a subsequent review of morphological changes based on our personal archive.<ul><li><span>1.</span><span><div>AC - Doxorubicin (Adriamycin) + Cyclophosphamide</div></span></li><li><span>2.</span><span><div>CaMKII - Calcium/Calmodulin-dependent protein kinase II</div></span></li><li><span>3.</span><span><div>Circ-INSR - Circulating Insulin Receptor</div></span></li><li><span>4.</span><span><div>CVDs - Cardiovascular Diseases</div></span></li><li><span>5.</span><span><div>CP – Cardioprotector</div></span></li><li><span>6.</span><span><div>GLUT - Glucose Transporter</div></span></li><li><span>7.</span><span><div>HF – Heart Failure</div></span></li><li><span>8.</span><span><div>ICAM - Intercellular Adhesion Molecule</div></span></li><li><span>9.</span><span><div>IL - Interleukin</div></span></li><li><span>10.</span><span><div>IκBα - Inhibitor of kappa B alpha</div></span></li><li><span>11.</span><span><div>MMP - Matrix Metalloproteinase</div></span></li><li><span>12.</span><span><div>MyD88 - Myeloid Differentiation Primary Response 88</div></span></li><li><span>13.</span><span><div>NADP+ - Nicotinamide Adenine Dinucleotide Phosphate</div></span></li><li><span>14.</span><span><div>NADPH - Nicotinamide Adenine Dinucleotide Phosphate Hydrogen</div></span></li><li><span>15.</span><span><div>NF-κB - Nuclear Factor kappa B</div></span></li><li><span>16.</span><span><div>NLRP3 - Nucleotide-binding domain, leucine-rich repeat containing protein 3</div></span></li><li><span>17.</span><span><div>NOS - Nitric Oxide Synthase</div></span></li><li><span>18.</span><span><div>Nrf2 - Nuclear factor erythroid 2-related factor 2</div></span></li><li><span>19.</span><span><div>NT-proBNP - N-terminal pro-B-type natriuretic peptide</div></span></li><li><span>20.</span><span><div>PLN - Phospholamban</div></span></li><li><span>21.</span><span><div>RyR - Ryanodine receptor</div></span></li><li><span>22.</span><span><div>SERCA2a - Sarco/Endoplasmic Reticulum Calcium ATPase 2a</div></span></li><li><span>23.</span><span><div>Sirt3 - Sirtuin 3</div></span></li><li><span>24.</span><span><div>SMAD3 - Mothers Against Decapentaplegic Homolog 3</div></span></li><li><span>25.</span><span><div>TGF-β1 - Transforming Growth Factor beta 1</div></span></li><li><span>26.</span><span><div>TLR4 - Toll-like receptor 4</div></span></li><li><span>27.</span><span><div>TNF-α - Tumor Necrosis Factor alpha</div></span></li><li><span>28.</span><span><div>VCAM - Vascular Cell Adhesion Molecule</div></span></li></ul></div></div>","PeriodicalId":51006,"journal":{"name":"Current Problems in Cardiology","volume":"50 1","pages":"Article 102882"},"PeriodicalIF":3.0000,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Current Problems in Cardiology","FirstCategoryId":"3","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S0146280624005176","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CARDIAC & CARDIOVASCULAR SYSTEMS","Score":null,"Total":0}
引用次数: 0
Abstract
Over the past 70 years, there has been extensive research focused on preventing chemotherapy-related cardiovascular complications. However, the current state of cardio-oncology research has raised more questions than answers. Experimental studies often present data that are difficult to compare and, at times, contradictory. One notable limitation in translating experimental findings to clinical practice is the reliance on models that administer only one chemotherapeutic drug to experimental animals, despite the common use of multidrug cancer treatments in real clinical settings. This article aims to discuss our own experience in modeling an experimental rat model of cardiomyopathy induced by the administration of two chemotherapeutic drugs, doxorubicin (adriamycin) and cyclophosphamide (AC mode of chemotherapy) – Avagimyan A., et al model, along with a subsequent review of morphological changes based on our personal archive.
1.
AC - Doxorubicin (Adriamycin) + Cyclophosphamide
2.
CaMKII - Calcium/Calmodulin-dependent protein kinase II
期刊介绍:
Under the editorial leadership of noted cardiologist Dr. Hector O. Ventura, Current Problems in Cardiology provides focused, comprehensive coverage of important clinical topics in cardiology. Each monthly issues, addresses a selected clinical problem or condition, including pathophysiology, invasive and noninvasive diagnosis, drug therapy, surgical management, and rehabilitation; or explores the clinical applications of a diagnostic modality or a particular category of drugs. Critical commentary from the distinguished editorial board accompanies each monograph, providing readers with additional insights. An extensive bibliography in each issue saves hours of library research.