Dear Colleagues,

The development of new drugs and innovative therapeutic strategies during the last decade has allowed patients to survive for longer following diagnosis of cancer than in the past. However, some anticancer drugs have cardiotoxic effects, which occur during or after treatment and can lead to the death of patients independently from the outcomes of oncologic therapy. Thus, the patients undergoing treatment with these drugs have a high risk of developing cardiovascular diseases and, consequently, to die from the side effects of the therapy rather than from the cancer. The discovery of the molecular mechanisms involved in cardiac responses to cardiotoxic drugs, which are still poorly known, represents the current goal of the cardio-oncology research aimed at preventing or treating cardiotoxicity. Over the years, this field of research has experienced progressively growing interest in identifying the molecular mechanisms underpinning the cardiotoxic effects of anticancer treatments, novel molecular targets to allow the design and development of novel biological therapeutic strategies, and early markers of cardiotoxicity toward preventing cardiac damage or to for promptly initiating effective therapy. Several targets involved in both the development of cardiovascular disease and cancer have been identified, including but not limited to GRKs, TLR, NFκB, and GPCR. Cardiomyocytes are generally the research target in these studies, but the functional contribution of non-myocyte cardiac cells is also receiving growing interest considering the functional crosstalk between the different types of cardiac cells. Among them, the influence of both resident and infiltrating immune cells as well as the contribution of fibroblasts and endothelial cells is fundamental in pathologic cardiac remodeling. This cellular crosstalk could be impaired by anticancer treatments, contributing to the exacerbation of cardiomyocyte damage. We welcome contributions that could increase the knowledge in the field and lead to ideas for the development of novel diagnostic and therapeutic strategies.

Dr. Daniela Sorriento
Prof. Dr. Guido Iaccarino
Guest Editors

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• cardiotoxicity
• molecular mechanisms of cardiac damage
• intracellular signaling
• inflammatory pathways
• GPCR
• NFκB signaling
• GRKs