Molecular mechanisms of doxorubicin-induced cardiotoxicity: novel roles of sirtuin 1-mediated signaling pathways

Zhang, Jingjing; Xiao, Mengjie; Wang, Shudong; Wang, Jie; Guo, Yuanfang; Tang, Yufeng; Gu, Junlian

doi:10.1007/s00018-020-03729-y

Cited by 55 publications

(29 citation statements)

References 166 publications

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“…Sufficient evidence revealed that DOX-induced cardiotoxicity is closely associated with increased oxidative stress in cardiomyocytes. DOX accumulation rapidly increases mitochondrial ROS production in cardiomyocytes by redox cycling, which damages mitochondrial function and then leads to more sustained oxidative stress [ 46 , 47 ]. Here, we observed that SIRT1 activation obviously alleviated oxidative stress by promoting nuclear NRF2 accumulation and function in DOX-treated cardiomyocytes, whereas the deletion of Sirt1 exacerbated DOX-induced oxidative stress ( Figs.…”

Section: Discussionmentioning

confidence: 99%

Cardiac SIRT1 ameliorates doxorubicin-induced cardiotoxicity by targeting sestrin 2

Tang

Zhang

et al. 2022

Redox Biology

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Section: Discussionmentioning

confidence: 99%

Cardiac SIRT1 ameliorates doxorubicin-induced cardiotoxicity by targeting sestrin 2

Tang

Zhang

et al. 2022

Redox Biology

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“…It is important to find improved methods, for DOX transportation and administration, considering drug efficacy and better selectivity between cancers among healthy cells. The design of nanopharmaceutical carriers is an important drug administration efficiency, and its pharmaceutical activity [6][7][8][9]; ref. SI1.…”

Section: Introductionmentioning

confidence: 99%

Quantum–mechanical characterization of the doxorubicin molecule to improve its anticancer functions

López-Chávez¹,

Garcia-Quiroz²,

Santiago-Jiménez

et al. 2021

MRS Advances

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We are presenting results based on the density-functional theory, DFT, in order to obtain stable structures of the doxorubicin molecule that may lead for healthier ways to inhibit cancer cells for humans. We obtained several electrochemical properties; such as electronic affinity, chemical potential, chemical hardness, electrophilicity index, and ionization potential. The maximum reactivity zone of a molecule is obtained founding its HOMO-LUMO boundary molecular orbitals and reactive sites were determined by Fukui indices. The distribution of electric charges and Mulliken population were obtained to determine areas and sites with excess or deficit of electrons. The Raman spectrum was theoretically obtained. The information presented would be very useful for possible new anticancer drugs.

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“…Conversely, SIRT1 inhibits DOX-induced mitochondrial dysfunction and cell death [51], and the overexpression of SIRT1 suppresses DOX-induced apoptosis and ROS production [52]. In addition, SIRT1 can deacetylate PGC-1α, activating a suite of genes [50] involved in mitochondrial function and biogenesis, such as nuclear respiratory factor-1 (Nrf1) [49,53]. Consistent with this, a recent study showed that NRF1 could protect human-induced pluripotent stem cells (hiPSC)-derived cardiomyocytes against a range of cardiotoxins, including DOX [54].…”

Section: Dox Accumulates In the Mitochondria And Perturbs Mitochondri...mentioning

confidence: 99%

Mitochondrial-Targeted Therapy for Doxorubicin-Induced Cardiotoxicity

Leung

Poon

2022

IJMS

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Anthracyclines, such as doxorubicin, are effective chemotherapeutic agents for the treatment of cancer, but their clinical use is associated with severe and potentially life-threatening cardiotoxicity. Despite decades of research, treatment options remain limited. The mitochondria is commonly considered to be the main target of doxorubicin and mitochondrial dysfunction is the hallmark of doxorubicin-induced cardiotoxicity. Here, we review the pathogenic mechanisms of doxorubicin-induced cardiotoxicity and present an update on cardioprotective strategies for this disorder. Specifically, we focus on strategies that can protect the mitochondria and cover different therapeutic modalities encompassing small molecules, post-transcriptional regulators, and mitochondrial transfer. We also discuss the shortcomings of existing models of doxorubicin-induced cardiotoxicity and explore advances in the use of human pluripotent stem cell derived cardiomyocytes as a platform to facilitate the identification of novel treatments against this disorder.

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Molecular mechanisms of doxorubicin-induced cardiotoxicity: novel roles of sirtuin 1-mediated signaling pathways

Cited by 55 publications

References 166 publications

Cardiac SIRT1 ameliorates doxorubicin-induced cardiotoxicity by targeting sestrin 2

Cardiac SIRT1 ameliorates doxorubicin-induced cardiotoxicity by targeting sestrin 2

Quantum–mechanical characterization of the doxorubicin molecule to improve its anticancer functions

Mitochondrial-Targeted Therapy for Doxorubicin-Induced Cardiotoxicity

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