Protective role of cezanne in doxorubicin-induced cardiotoxicity by inhibiting autophagy, apoptosis and oxidative stress

Zhang, Jiayan; Zha, Yafang; Jiao, Yuchen; Li, Yanyan; Zhang, Song

doi:10.1016/j.tox.2023.153426

Cited by 13 publications

(5 citation statements)

References 46 publications

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“…However, paradoxically, excessive cardiomyocyte cell death can occur because of the impairment of autophagy rather than its activation during DOX treatment. 44,45 Autophagy begins with activation of the 5' adenosine monophosphate-activated protein kinase pathway and inhibition of the mammalian target of rapamycin pathway. 46 This is a signal that autophagic precursors germinate from the endoplasmic reticulum, accompanied by the formation of an initial complex composed of unc-51-like kinase 1, rb1-induced curl protein 1 and Atg.…”

Section: Discussionmentioning

confidence: 99%

“…DOX can induce cellular stress conditions that may activate autophagy. However, paradoxically, excessive cardiomyocyte cell death can occur because of the impairment of autophagy rather than its activation during DOX treatment 44,45 . Autophagy begins with activation of the 5' adenosine monophosphate‐activated protein kinase pathway and inhibition of the mammalian target of rapamycin pathway 46 .…”

Section: Discussionmentioning

confidence: 99%

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Ligustrazine and liguzinediol protect against doxorubicin‐induced cardiomyocytes injury by inhibiting mitochondrial apoptosis and autophagy

Lian,

Tong,

Zhu

et al. 2023

Clin Exp Pharma Physio

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Preventing or treating heart failure (HF) by blocking cardiomyocyte apoptosis is an effective strategy that improves survival and reduces ventricular remodelling and dysfunction in the chronic stage. Autophagy is a mechanism that degrades intracellular components and compensates for energy deficiency, which is commonly observed in cardiomyocytes of failed hearts. Cardiomyocytes activated by doxorubicin (DOX) exhibit strong autophagy. This study aims to investigate the potential protective effect of ligustrazine and its derivative liguzinediol on regulating DOX‐induced cardiomyocyte apoptosis and explore the use of the embryonic rat heart‐derived myoblast cell line H9C2 for identifying novel treatments for HF. The results indicated that it has been demonstrated to reverse myocardial infarction remodelling in failed hearts by promoting autophagy in salvaged cardiomyocytes and anti‐apoptosis of cardiomyocytes in granulation tissue. Our study suggests that ligustrazine and liguzinediol can be a promising agents and autophagy is potential pathway in the management of HF.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Ligustrazine and liguzinediol protect against doxorubicin‐induced cardiomyocytes injury by inhibiting mitochondrial apoptosis and autophagy

Lian,

Tong,

Zhu

et al. 2023

Clin Exp Pharma Physio

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“…However, its benefit is limited by a series of side effects such as induction of apoptosis on cardiomyocytes and over production of reactive oxygen species. 20 The drug efflux function of P-gp and anti-apoptotic function of heat shock protein (HSP) are well-known elements that decrease the sensitivity of cancer cells to ADR. Therefore, inhibitors of P-gp and HSP may be able to reduce ADR dosage in tumor therapy to preventing side effects.…”

Section: Figure 1 the Chemical Structures Of The Isolated Compounds P...mentioning

confidence: 99%

Chemical Structures and Cell Death Inducing Activities of the Metabolites of Aspergillus terreus

Μatsumoto¹,

Watanabe²,

Okayama³

et al. 2023

HETEROCYCLES

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A new steroid, terreus steroid (1), and eight known compounds (2-9) have been isolated from the airborne-derived fungus Aspergillus terreus. The structure of terreus steroid (1) was elucidated based on the chemical/physicochemical evidence. The cell death-inducing activities of the isolated compounds with or without Adriamycin (ADR) were observed using time-lapse cell imaging. Among the isolated compounds, terreus steroid (1) and territrem B (3) significantly reduced the number of mitotic entry cells at 60 μM. In addition, terreus steroid (1), territrem C (2), territrem B (3), epi-aszonalenin A (5), and methyl 3,4,5-trimethoxy-2-(2-(nicotinamido)benzamido)benzoate (6) significantly increased the number of dead cells on Adriamycin-treated HeLa cells.

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“…Some studies have reported that anthracyclines induce autophagy [ 28 ], while others have reported that anthracyclines inhibit autophagy [ 32 , 33 ]. Similarly, studies on the effects of genetic or pharmacological suppression of autophagy have yielded mixed results, with some indicating protective effects [ 34 , 35 ], while others demonstrate that sustained reduction of autophagy cannot maintain protection against DOXIC [ 36 , 37 ].…”

Section: Autophagymentioning

confidence: 99%

Recent Advances in the Mechanisms of Cell Death and Dysfunction in Doxorubicin Cardiotoxicity

Wang,

Ma,

Gao

et al. 2023

Rev. Cardiovasc. Med.

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Despite recent advances in cancer therapy, anthracycline-based combination therapy remains the standardized first-line strategy and has been found to have effective antitumor actions. Anthracyclines are extremely cardiotoxic, which limits the use of these powerful chemotherapeutic agents. Although numerous studies have been conducted on the cardiotoxicity of anthracyclines, the precise mechanisms by which doxorubicin causes cardiomyocyte death and myocardial dysfunction remain incompletely understood. This review highlights recent updates in mechanisms and therapies involved in doxorubicin-induced cardiomyocyte death, including autophagy, ferroptosis, necroptosis, pyroptosis, and apoptosis, as well as mechanisms of cardiovascular dysfunction resulting in myocardial atrophy, defects in calcium handling, thrombosis, and cell senescence. We sought to uncover potential therapeutic approaches to manage anthracycline cardiotoxicity via manipulation of crucial targets involved in doxorubicin-induced cardiomyocyte death and dysfunction.

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Protective role of cezanne in doxorubicin-induced cardiotoxicity by inhibiting autophagy, apoptosis and oxidative stress

Cited by 13 publications

References 46 publications

Ligustrazine and liguzinediol protect against doxorubicin‐induced cardiomyocytes injury by inhibiting mitochondrial apoptosis and autophagy

Ligustrazine and liguzinediol protect against doxorubicin‐induced cardiomyocytes injury by inhibiting mitochondrial apoptosis and autophagy

Chemical Structures and Cell Death Inducing Activities of the Metabolites of Aspergillus terreus

Recent Advances in the Mechanisms of Cell Death and Dysfunction in Doxorubicin Cardiotoxicity

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