Figure 1.

Mechanisms underlying chemotherapy induced heart failure (CIHF). 1st hit: interference with different pathways (among others: VEGF, vascular endothelial growth factor; HER2, human epidermal growth factor receptor 2), associated sub-receptor tyrosine kinases (TKI) and basic cellular systems (UPS, ubiquitin-proteasome-system) leads to distinct molecular effects predisposing to cardiotoxicity. 2nd hit: together with the individual cardiovascular comorbidity, systemic extracardiac effects of certain therapeutics increase cardiac stress. Both hits are essential for the development of CIHF.