Doxorubicin-induced cardiotoxicity: An update on the molecular mechanism and novel therapeutic strategies for effective management

2021/05/13 by Pushkar Singh Rawat, Aiswarya Jaiswal, Amit Khurana +2 · 6 citations
Medicine · #Cancer Treatment and Pharmacology #Cancer-related cognitive impairment studies #Chemotherapy-induced cardiotoxicity and mitigation

paper · doi:10.1016/j.biopha.2021.111708

openalex publication_date 2021/05/13 · openalex created_date 2025/10/10 · openalex updated_date 2026/07/30

Abstract

homeostasis, autophagy, the release of nitric oxide and inflammatory mediators and altered gene and protein expression that involved apoptosis. Dox also causes downregulation of DNA methyltransferase 1 (DNMT1) enzyme activity which leads to a reduction in the DNA methylation process. This hypomethylation causes dysregulation in the mitochondrial genes like peroxisome proliferator-activated receptor-gamma coactivator (PGC)-1-alpha (PGC-1α), nuclear respiratory factor 1 (NRF-1) and mitochondrial transcription factor A (TFAM) unit in the heart. Apart from DNA methylation, Dox treatment also alters the micro RNAs levels and histone deacetylase (HDAC) activity. Therefore, in the current review, we have provided a detailed update on the current understanding of the pathological mechanisms behind the well-known Dox-induced cardiotoxicity. Further, we have provided some of the most plausible pharmacological strategies which have been tested against Dox-induced cardiotoxicity.

Citations

• Doxorubicin-induced cardiomyopathy: From molecular mechanisms to therapeutic strategies
• Anthracyclines: Molecular Advances and Pharmacologic Developments in Antitumor Activity and Cardiotoxicity

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