Editorial: Novel mechanisms, imaging approaches, and management strategies for anthracycline-induced cardiotoxicity

Packard, René R. Sevag; Yang, Eric H.

doi:10.3389/fcvm.2022.1109078

Cited by 1 publication

(2 citation statements)

References 8 publications

(7 reference statements)

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“…With the development of the detection technology, echocardiography, cardiac computed tomography, cardiac magnetic resonance imaging, nuclear and molecular cardiology and monitoring strategies for cardiac biomarkers have been progressively applied in clinical practice to facilitate early diagnosis and treatment of patients [6]. Biomarkers used to detect DOX-induced cardiomyopathy include cardiac troponin I (cTnI), hypersensitive troponin I, creatine kinase isoenzyme (CK-MB), type B brain natridium peptide (BNP) and NT-pro BNP [7].…”

Section: Introductionmentioning

confidence: 99%

“…The current clinical treatment strategies for DOXinduced cardiomyopathy are mainly to limit the cumulative dose of DOX, the use of liposomal doxorubicin and the application of cardioprotective drugs, including Dexrazoxane, angiotensin converting enzyme inhibitor (ACEI), angiotensin receptor blocker (ARB), mineralocorticoid receptor antagonist (MRA), β-blockers (BB) and statins [6,8]. Dexrazoxane (DEX) is the only drug currently approved to prevent DOX-induced cardiomyopathy by inhibiting topoisomerase IIβ and DOX-Fe 2+ complex [9].…”

Section: Introductionmentioning

confidence: 99%

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Role of oxidative stress and inflammation-related signaling pathways in doxorubicin-induced cardiomyopathy

et al. 2023

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Doxorubicin (DOX) is a powerful and commonly used chemotherapeutic drug, used alone or in combination in a variety of cancers, while it has been found to cause serious cardiac side effects in clinical application. More and more researchers are trying to explore the molecular mechanisms of DOX-induced cardiomyopathy (DIC), in which oxidative stress and inflammation are considered to play a significant role. This review summarizes signaling pathways related to oxidative stress and inflammation in DIC and compounds that exert cardioprotective effects by acting on relevant signaling pathways, including the role of Nrf2/Keap1/ARE, Sirt1/p66Shc, Sirt1/PPAR/PGC-1α signaling pathways and NOS, NOX, Fe2+ signaling in oxidative stress, as well as the role of NLRP3/caspase-1/GSDMD, HMGB1/TLR4/MAPKs/NF-κB, mTOR/TFEB/NF-κB pathways in DOX-induced inflammation. Hence, we attempt to explain the mechanisms of DIC in terms of oxidative stress and inflammation, and to provide a theoretical basis or new idea for further drug research on reducing DIC.

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Section: Introductionmentioning

confidence: 99%