Revisiting treatment-related cardiotoxicity in patients with malignant lymphoma—a review and prospects for the future

Figures

• 

  Figure 1. Mechanisms of anthracycline-induced cardiotoxicity with highlighted possible therapeutic targets. Anthracycline cytotoxic effects in cell include DNA alterations [direct damage and processing alterations through inhibition of cardiac TOP2beta (14)], energy metabolism impairment, induction of apoptosis [via casp3, p53 and p38 pathway (25, 35, 39)], and decreased contractility [involvement of MURF1 pathway and myosin heavy chain degradation (56, 57)]. Cell parts illustrations were implemented from free Servier repository available at: https://smart.servier.com/.

• 

  Figure 2. Mechanism of CTX-induced cardiomyopathy and its possible pharmacoprevention. CTX cytotoxic properties are similar to those of anthracyclines to a certain degree as both drugs direct several similar cellular compartments including mitochondria (energy metabolism) (99) and myosin heavy chains (MURF1) (111). Moreover, CTX cardiac adverse events are mediated through signal impairment (METTL3 downregulation), vasospasm (inhibition of NOS), interstitial haemorrhage (induced through direct cell damage and formation of microthrombi), inflammation (upregulation of NF-kappa-B), oxidative stress and apoptosis (103–105). Cell parts illustrations were implemented from free Servier repository available at: https://smart.servier.com/.