Department of Cardiology, School of Medicine, Atherosclerosis Research Center, Golestan Hospital, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran.
Shiraz University of Medical Science, Shiraz, Iran.
Mol Biotechnol. 2023 Sep;65(9):1403-1413. doi: 10.1007/s12033-023-00697-z. Epub 2023 Feb 27.
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.
癌症是一种仍无法完全治愈的疾病；现有的治疗方法伴随着许多并发症，使其更加复杂。癌细胞转移的原因之一是上皮间质转化（EMT）。最近的研究表明，EMT 会导致心肌毒性和心脏病，如心力衰竭、肥大和纤维化。本研究评估了通过 EMT 导致心肌毒性的分子和信号通路。研究表明，炎症、氧化应激和血管生成过程参与了 EMT 和心肌毒性。与这些过程相关的途径起着双刃剑的作用。就炎症和氧化应激而言，分子途径导致心肌细胞凋亡和心肌毒性诱导。而血管生成过程抑制了 EMT 的进展，但却抑制了心肌毒性。另一方面，一些分子途径，如 PI3K/mTOR，尽管导致 EMT 的进展，但会导致心肌细胞的增殖，并防止心肌毒性。因此，结论是鉴定分子途径有助于设计治疗和预防策略，以提高患者的生存率。
