Journal
MOLECULES
Volume 28, Issue 11, Pages -Publisher
MDPI
DOI: 10.3390/molecules28114294
Keywords
doxorubicin; Toll-like receptor 4; cardiotoxicity; heart
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Doxorubicin (Dox) is commonly used chemotherapeutic drug, but its cardiotoxicity reduces its therapeutic efficacy. Dox-induced cardiac inflammation is considered as one of the underlying mechanisms involved in Dox-induced cardiotoxicity. Understanding the role of the Toll-like receptor 4 (TLR4) signaling pathway in Dox-induced cardiac inflammation might be beneficial for developing potential therapeutic strategies.
Doxorubicin (Dox) is one of the most frequently used chemotherapeutic drugs in a variety of cancers, but Dox-induced cardiotoxicity diminishes its therapeutic efficacy. The underlying mechanisms of Dox-induced cardiotoxicity are still not fully understood. More significantly, there are no established therapeutic guidelines for Dox-induced cardiotoxicity. To date, Dox-induced cardiac inflammation is widely considered as one of the underlying mechanisms involved in Dox-induced cardiotoxicity. The Toll-like receptor 4 (TLR4) signaling pathway plays a key role in Dox-induced cardiac inflammation, and growing evidence reports that TLR4-induced cardiac inflammation is strongly linked to Dox-induced cardiotoxicity. In this review, we outline and address all the available evidence demonstrating the involvement of the TLR4 signaling pathway in different models of Dox-induced cardiotoxicity. This review also discusses the effect of the TLR4 signaling pathway on Dox-induced cardiotoxicity. Understanding the role of the TLR4 signaling pathway in Dox-induced cardiac inflammation might be beneficial for developing a potential therapeutic strategy for Dox-induced cardiotoxicity.
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