Ferroptosis: A novel therapeutic target of natural products against doxorubicin-induced cardiotoxicity - 21/08/24
Abstract |
Doxorubicin (DOX), a commonly used chemotherapy drug, is hindered due to its tendency to induce cardiotoxicity (DIC). Ferroptosis, a novel mode of programmed cell death, has received substantial attention for its involvement in DIC. Recently, natural product-derived ferroptosis regulator emerged as a potential strategy for treating DIC. In this review, a comprehensive search was conducted across PubMed, Web of Science, Google Scholar, and ScienceDirect databases to gather relevant articles on the use of natural products for treating DIC in relation to ferroptosis. The available papers were carefully reviewed to summarize the therapeutic effects and underlying mechanisms of natural products in modulating ferroptosis for DIC treatment. It was found that ferroptosis plays an important role in DIC pathogenesis, with dysregulated expression of ferroptosis-related proteins strongly implicated in the condition. Natural products, such as flavonoids, polyphenols, terpenoids, and quinones can act as GPX4 activators, Nrf2 agonists, and lipid peroxidation inhibitors, thereby enhancing cell viability, attenuating myocardial fibrosis, improving cardiac function, and suppressing ferroptosis in both in vitro and in vivo models of DIC. This review demonstrates a strong correlation between DOX-induced cardiac ferroptosis and key proteins, such as GPX4, Keap1, Nrf2, AMPK, and HMOX1. Natural products are likely to exert therapeutic effects against DIC by modulating the activity of these proteins.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
Highlights |
• | Ferroptosis plays a vital role in the pathogenesis of doxorubicin-induced cardiotoxicity. |
• | Targeting ferroptosis as a promising therapeutic strategy for doxorubicin-induced cardiotoxicity. |
• | Natural products hold potential as ferroptosis regulators in doxorubicin-induced cardiotoxicity. |
• | Diverse therapeutic effects and multifaceted mechanisms of natural products in ferroptosis modulation. |
Abbreviations : ACC, ACSL4, AIFM2, AKT, AMPK, AMPKα2, ARE, AT1R, CHIP, CoA, CoQ10, CoQ10H2, DIC, DKK1, DOX, EP1, FoxO1, FSP1, FTH1, GPX4, GSDMD, GSH, GSSG, GSTP1, HMOX1, HO-1, HSF1, IGF-IIR, Keap1, LDH, MAPK, MDA, MDM2, MITOL, NF-κB, NLRP3, NOX2, NOX4, NQO1, Nrf2, O2●−, OH●, PI3K, PRMT4, PTGS2, PUFA, QKI, ROS, SD, SIRT1, SLC40A1, SLC7A11, TCM, TLR4, Trf, TRIM21, TRPA1, YAP
Keywords : Natural products, Ferroptosis, Doxorubicin, Cardiotoxicity, Molecular mechanism
Plan
Vol 178
Article 117217- septembre 2024 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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