The Role of Epithelial Mesenchymal Transition (EMT) in Pathogenesis of Cardiotoxicity: Diagnostic & Prognostic Approach.

Cancer is one of the diseases, which it is not still completely curable; the existing treatments are associated with many complications, that double its complexity. One of the causes of cancer cell metastasis is Epithelial Mesenchymal Transition (EMT). Recently study demonstrated that EMT cause cardiotoxicity and heart diseases such as heart failure, hypertrophy and fibrosis. This study evaluated molecular and signaling pathway, which lead to cardiotoxicity via EMT. It was demonstrated that the processes of inflammation, oxidative stress and angiogenesis were involved in EMT and cardiotoxicity. The pathways related to these processes act as a double-edged sword. In relation to inflammation and oxidative stress, molecular pathways caused apoptosis of cardiomyocytes and cardiotoxicity induction. While the angiogenesis process inhibits cardiotoxicity despite the progression of EMT. On the other hand, some molecular pathways such as PI3K/mTOR despite causing the progression of EMT lead to the proliferation of cardiomyocytes and prevent cardiotoxicity. Therefore, it was concluded that the identification of molecular pathways can help in designing therapeutic and preventive strategies to increase patients' survival.