A n t h r a c y c l i n e s , i n c l u d i n g d o x o r u b i c i n t h a t w a s discovered in Italy over a half century ago, are widely used chemotherapeutics for the treatment of many human cancers (1). Shortly after their introduction, the cardiovascular toxicity has been reported (2), but despite decades of research, the pathogenesis of cardiotoxicity is still incompletely understood. Contrary to the common perception, the dimension of anthracycline cardiotoxicity is by no means small. A

more »

... recent analysis, conducted on patients treated with anthracyclines with a follow-up of 9 years, reported a rate of 17.9% and 6.3% of subclinical and overt cardiotoxicity, respectively (3). The use of alternative echocardiographic parameters such as myocardial strain, documented even higher incidence of anthracycline-induced cardiac dysfunction, rating about 30% in adult survivors of childhood cancer (4). Given the growing population of cancer survivors exposed to the treatment as children or adults, cardiotoxicity has attracted more attention in the new discipline of cardio-oncology. This recent initiative aims at promoting research of mechanisms driving cardiotoxicity and bringing uniformity to the guidelines regarding diagnosis, management and monitoring (5). In a recently published Circulation Research paper, Gupta and colleagues reported a previously unrecognized phenomenon involved in the pathogenesis of anthracycline cardiotoxicity (6). By global transcriptional profiling approach, the researchers identified doxorubicin-induced alterations in the levels of several cardiac RNA-binding proteins (RBPs). In particular, the downregulation of Quaking isoform 5 (Qki5) was observed. RBPs are known to control the function of coding and noncoding RNAs.