We report the unique case of a patient who recovered cardiac function despite a history of doxorubicin-induced cardiomyopathy, chest radiation therapy, high dose chemotherapy post-allogeneic stem cell transplant, and triplet pregnancy. Data are sparse on doxorubicin-induced cardiomyopathy in pregnant patients, calling for further studies to help formulate management or surveillance recommendations. ().
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http://dx.doi.org/10.1016/j.jaccas.2020.04.020 | DOI Listing |
Nat Commun
January 2025
Shanghai Frontiers Science Center of Genome Editing and Cell Therapy, Shanghai Key Laboratory of Regulatory Biology, Institute of Biomedical Sciences and School of Life Sciences, East China Normal University, Shanghai, 200241, China.
Energy deprivation and metabolic rewiring of cardiomyocytes are widely recognized hallmarks of heart failure. Here, we report that HEY2 (a Hairy/Enhancer-of-split-related transcriptional repressor) is upregulated in hearts of patients with dilated cardiomyopathy. Induced Hey2 expression in zebrafish hearts or mammalian cardiomyocytes impairs mitochondrial respiration, accompanied by elevated ROS, resulting in cardiomyocyte apoptosis and heart failure.
View Article and Find Full Text PDFCell Commun Signal
December 2024
Department of Cardiology, The Second Affiliated Hospital of Jiaxing University, Jiaxing, Zhejiang, China.
Anthracycline antitumor drug doxorubicin (DOX) induces severe cardiotoxicity. Deubiquitinating enzymes (DUBs) are crucial for protein stability and function and play a significant role in cardiac pathophysiology. By comparing RNA sequencing datasets and conducting functional screening, we determined that Myb-like, SWIRM, and MPN domains 1 (MYSM1) is a key regulator of DOX-induced cardiotoxicity.
View Article and Find Full Text PDFEur J Med Chem
February 2025
Wuxi School of Medicine & Wuxi Mental Health Center, Jiangnan University, Wuxi, 214122, China. Electronic address:
Doxorubicin (DOX)-induced cardiomyopathy (DIC) greatly limits its clinical application of the anticancer drug. Therefore, there is an immediate necessity to undertake intervention studies to minimize DIC, encompassing the screening of regulatory compounds and delving into the underlying regulatory mechanisms. A growing body of research suggests that ferroptosis is an essential process in the development of DIC.
View Article and Find Full Text PDFInt J Mol Sci
November 2024
Department of Forensic Medicine, School of Basic Medicine, Soochow University, Suzhou 215123, China.
Mutual interaction between doxorubicin (DOX) and cardiomyocytes is crucial for cardiotoxicity progression. Cardiomyocyte injury is an important pathological feature of DOX-induced cardiomyopathy, and its molecular pathogenesis is multifaceted. In addition to the direct toxic effects of DOX on cardiomyocytes, DOX-induced exosomes in the extracellular microenvironment also regulate the pathophysiological states of cardiomyocytes.
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