A review of the pathophysiological mechanisms of doxorubicin-induced cardiotoxicity and aging

Abstract

The population of cancer survivors is rapidly increasing due to improving healthcare. However, cancer therapies often have long-term side effects. One example is cancer therapy-related cardiac dysfunction (CTRCD) caused by doxorubicin: up to 9% of the cancer patients treated with this drug develop heart failure at a later stage. In recent years, doxorubicin-induced cardiotoxicity has been associated with an accelerated aging phenotype and cellular senescence in the heart. In this review we explain the evidence of an accelerated aging phenotype in the doxorubicin-treated heart by comparing it to healthy aged hearts, and shed light on treatment strategies that are proposed in pre-clinical settings. We will discuss the accelerated aging phenotype and the impact it could have in the clinic and future research.

The sGCa Vericiguat Exhibit Cardioprotective and Anti-Sarcopenic Effects through NLRP-3 Pathways: Potential Benefits for Anthracycline-Treated Cancer Patients

“…Anthracycline-mediated cardiovascular injuries involve high intracellular calcium levels [39]. Intracellular Ca ++ in human cardiomyocytes and muscle cells was quantified through the fluorescence dye Fluo-3 AM, according to the manufacturer's protocol.…”

The Potential Regenerative Effect of L-carnitine Pretreated Mesenchymal Stem Cells in Myocardial Infarction Through Modulating Apoptosis, Inflammation, and Cellular Differentiation

“…The treatment of myocardial infarction primarily relies on swift reperfusion and reopening of the blocked vessels to save injured cardiomyocytes, reduce infarct size, and restore myocardial tissue [5][6][7]. Cancer drug therapy is one of the principal sources of cardiac side effects and cancer therapy-related cardiac dysfunction (CTRCD) [8][9][10]. One of these chemotherapeutic drugs is Doxorubicin (DOX).…”