Carnosic acid protects against doxorubicin-induced cardiotoxicity through enhancing the Nrf2/HO-1 pathway

Huang, Shan; Wu, Gang; Liu, Beilei; Yang, Manqi; Mao, Shuai; Ju, Hehua; Liu, Zheyu; Huang, Min

doi:10.1039/d2fo03904d

Cited by 14 publications

(1 citation statement)

References 38 publications

(44 reference statements)

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“…According to published studies, however, long-term administration of doxorubicin can cause severe damage to numerous organs in the body, with the heart being the primary target of doxorubicin toxicity [ 1 , 2 ]. Long-term administration of doxorubicin can cause structural alterations in the heart, most notably reduced left ventricular ejection fraction,arrhythmias, reduced ventricular wall thickness, increased ventricular internal diameter and even heart failure [ 3 – 11 ]. According to the most recent epidemiological data, however, up to 5% of patients will exhibit varying degrees of cardiotoxic manifestations after doxorubicin administration, and the toxic effects become more severe with increasing cumulative doses, with the probability of heart failure reaching 48% when the cumulative dose reaches 700 mg/m 2 [ 12 , 13 ].…”

Section: Introductionmentioning

confidence: 99%

Nrf2: a dark horse in doxorubicin-induced cardiotoxicity

Zhao¹,

Zheng²,

Sun³

et al. 2023

Cell Death Discov.

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Being a broad-spectrum anticancer drug, doxorubicin is indispensable for clinical treatment. Unexpectedly, its cardiotoxic side effects have proven to be a formidable obstacle. Numerous studies are currently devoted to elucidating the pathological mechanisms underlying doxorubicin-induced cardiotoxicity. Nrf2 has always played a crucial role in oxidative stress, but numerous studies have demonstrated that it also plays a vital part in pathological mechanisms like cell death and inflammation. Numerous studies on the pathological mechanisms associated with doxorubicin-induced cardiotoxicity demonstrate this. Several clinical drugs, natural and synthetic compounds, as well as small molecule RNAs have been demonstrated to prevent doxorubicin-induced cardiotoxicity by activating Nrf2. Consequently, this study emphasizes the introduction of Nrf2, discusses the role of Nrf2 in doxorubicin-induced cardiotoxicity, and concludes with a summary of the therapeutic modalities targeting Nrf2 to ameliorate doxorubicin-induced cardiotoxicity, highlighting the potential value of Nrf2 in doxorubicin-induced cardiotoxicity.

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Section: Introductionmentioning

confidence: 99%

Nrf2: a dark horse in doxorubicin-induced cardiotoxicity

Zhao¹,

Zheng²,

Sun³

et al. 2023

Cell Death Discov.

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Ferroptosis: Latest evidence and perspectives on plant‐derived natural active compounds mitigating doxorubicin‐induced cardiotoxicity

Wang,

Liu

et al. 2024

J of Applied Toxicology

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Doxorubicin (DOX) is a chemotherapy drug widely used in clinical settings, acting as a first‐line treatment for various malignant tumors. However, its use is greatly limited by the cardiotoxicity it induces, including doxorubicin‐induced cardiomyopathy (DIC). The mechanisms behind DIC are not fully understood, but its potential biological mechanisms are thought to include oxidative stress, inflammation, energy metabolism disorders, mitochondrial damage, autophagy, apoptosis, and ferroptosis. Recent studies have shown that cardiac injury induced by DOX is closely related to ferroptosis. Due to their high efficacy, availability, and low side effects, natural medicine treatments hold strong clinical potential. Currently, natural medicines have been shown to mitigate DOX‐induced ferroptosis and ease DIC through various functions such as antioxidation, iron ion homeostasis correction, lipid metabolism regulation, and mitochondrial function improvement. Therefore, this review summarizes the mechanisms of ferroptosis in DIC and the regulation by natural plant products, with the expectation of providing a reference for future research and development of inhibitors targeting ferroptosis in DIC.This review explores the mechanisms of ferroptosis in doxorubicin‐induced cardiomyopathy (DIC) and summarizes how natural plant products can alleviate DIC by inhibiting ferroptosis through reducing oxidative stress, correcting iron ion homeostasis, regulating lipid metabolism, and improving mitochondrial function.

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An Integrated Network Pharmacology and RNA-seq Approach for Exploring the Protective Effect of Andrographolide in Doxorubicin-Induced Cardiotoxicity

Liu,

et al. 2024

Cardiovasc Drugs Ther

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Carnosic acid protects against doxorubicin-induced cardiotoxicity through enhancing the Nrf2/HO-1 pathway

Abstract: Doxorubicin (DOX) is used extensively in anticancer therapy, but its clinical applications are limited due to cardiotoxicity. Carnosic acid (CA) is a bioactive compound found in rosemary. It has been...

Cited by 14 publications

References 38 publications

Nrf2: a dark horse in doxorubicin-induced cardiotoxicity

Nrf2: a dark horse in doxorubicin-induced cardiotoxicity

Ferroptosis: Latest evidence and perspectives on plant‐derived natural active compounds mitigating doxorubicin‐induced cardiotoxicity

An Integrated Network Pharmacology and RNA-seq Approach for Exploring the Protective Effect of Andrographolide in Doxorubicin-Induced Cardiotoxicity

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