The role of melatonin on doxorubicin-induced cardiotoxicity: A systematic review

Najafi, Masoud; Shayesteh, Mohammad Reza; Mortezaee, Keywan; Farhood, Bagher; Haghi‐Aminjan, Hamed

doi:10.1016/j.lfs.2019.117173

Cited by 78 publications

(47 citation statements)

References 113 publications

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“…Along with identification of molecular pathways, scientists have tried to develop synthetic drugs in their regulation. It is worth mentioning that plus to synthetic drugs, there has been a great trend toward plant derived-natural compounds in the regulation of molecular pathways and mechanisms (Najafi et al, 2019b;Mortezaee et al, 2020). Nowadays, researchers are more interested in naturally occurring compounds compared to synthetic therapeutics.…”

Section: Introductionmentioning

confidence: 99%

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

et al. 2020

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Immune response, proliferation, migration and angiogenesis are juts a few of cellular events that are regulated by transforming growth factor-β (TGF-β) in cells. A number of studies have documented that TGF-β undergoes abnormal expression in different diseases, e.g., diabetes, cancer, fibrosis, asthma, arthritis, among others. This has led to great fascination into this signaling pathway and developing agents with modulatory impact on TGF-β. Curcumin, a natural-based compound, is obtained from rhizome and roots of turmeric plant. It has a number of pharmacological activities including antioxidant, anti-inflammatory, anti-tumor, anti-diabetes and so on. Noteworthy, it has been demonstrated that curcumin affects different molecular signaling pathways such as Wnt/β-catenin, Nrf2, AMPK, mitogen-activated protein kinase and so on. In the present review, we evaluate the potential of curcumin in regulation of TGF-β signaling pathway to corelate it with therapeutic impacts of curcumin. By modulation of TGF-β (both upregulation and down-regulation), curcumin ameliorates fibrosis, neurological disorders, liver disease, diabetes and asthma. Besides, curcumin targets TGF-β signaling pathway which is capable of suppressing proliferation of tumor cells and invading cancer cells.

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Section: Introductionmentioning

confidence: 99%

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

et al. 2020

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“…Among the potential mechanisms that have been studied by many researchers, apoptosis is an important etiology and pathological process in DOX-induced cardiac injury [ 41 , 42 ]. Previous studies showed that DOX exposure at submicromolar concentrations caused apoptotic cell death in cardiomyocytes, and oxidative stress has been shown to be responsible for cardiac injury and cardiomyocyte apoptosis [ 43 , 44 ]. To detect the role of Prdx1 in DOX-induced cardiomyocyte apoptosis, western blotting and TUNEL staining were performed.…”

Section: Discussionmentioning

confidence: 99%

Peroxiredoxin-1 Overexpression Attenuates Doxorubicin-Induced Cardiotoxicity by Inhibiting Oxidative Stress and Cardiomyocyte Apoptosis

Jiang

Gong

et al. 2020

Oxidative Medicine and Cellular Longevity

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Background. Previous research has shown that peroxiredoxin 1 (Prdx1) is an important modulator of physiological and pathophysiological cardiovascular events. This study is aimed at investigating the role and underlying mechanism of Prdx1 in doxorubicin- (DOX-) induced cardiotoxicity. Cardiac-specific expression of Prdx1 was induced in mice, and the mice received a single dose of DOX (15 mg/kg) to generate cardiotoxicity. First, our study demonstrated that Prdx1 expression was upregulated in the heart and in cardiomyocytes after DOX treatment. Second, we provided direct evidence that Prdx1 overexpression ameliorated DOX-induced cardiotoxicity by attenuating oxidative stress and cardiomyocyte apoptosis. Mechanistically, we found that DOX treatment increased the phosphorylation level of apoptosis signal-regulating kinase-1 (ASK1) and the downstream protein p38 in the heart and in cardiomyocytes, and these effects were decreased by Prdx1 overexpression. In contrast, inhibiting Prdx1 promoted DOX-induced cardiac injury via the ASK1/p38 pathway. These results suggest that Prdx1 may be an effective therapeutic option to prevent DOX-induced cardiotoxicity.

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“…Nowadays, the application of naturally occurring compounds has undergone an increase for management of various chronic diseases [115,116]. This is due to the great pharmacological impacts of plant-derived chemicals that have made them appropriate options in the treatment of a variety of disorders such as cancer, diabetes [117], cardiovascular diseases [118], autoimmune diseases [119] and infectious diseases [120].…”

Section: Regulation Of Mitochondria By Plant-derived Chemicalsmentioning

confidence: 99%

“…There have been efforts to reveal the underlying mechanism of action of these agents [3,121]. It has been demonstrated that plant-derived chemicals are capable of affecting molecular signaling pathways and organelles in the treatment of diseases [3,4,115,121]. For instance, resveratrol can affect the ER to exert its therapeutic impacts [116].…”

Section: Regulation Of Mitochondria By Plant-derived Chemicalsmentioning

confidence: 99%

Natural products and phytochemical nanoformulations targeting mitochondria in oncotherapy: an updated review on resveratrol

et al. 2020

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Mitochondria are intracellular organelles with two distinct membranes, known as an outer mitochondrial membrane and inner cell membrane. Originally, mitochondria have been derived from bacteria. The main function of mitochondria is the production of ATP. However, this important organelle indirectly protects cells by consuming oxygen in the route of energy generation. It has been found that mitochondria are actively involved in the induction of the intrinsic pathways of apoptosis. So, there have been efforts to sustain mitochondrial homeostasis and inhibit its dysfunction. Notably, due to the potential role of mitochondria in the stimulation of apoptosis, this organelle is a promising target in cancer therapy. Resveratrol is a non-flavonoid polyphenol that exhibits significant pharmacological effects such as antioxidant, anti-diabetic, anti-inflammatory and anti-tumor. The anti-tumor activity of resveratrol may be a consequence of its effect on mitochondria. Multiple studies have investigated the relationship between resveratrol and mitochondria, and it has been demonstrated that resveratrol is able to significantly enhance the concentration of reactive oxygen species, leading to the mitochondrial dysfunction and consequently, apoptosis induction. A number of signaling pathways such as sirtuin and NF-κB may contribute to the mitochondrial-mediated apoptosis by resveratrol. Besides, resveratrol shifts cellular metabolism from glycolysis into mitochondrial respiration to induce cellular death in cancer cells. In the present review, we discuss the possible interactions between resveratrol and mitochondria, and its potential application in cancer therapy.

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The role of melatonin on doxorubicin-induced cardiotoxicity: A systematic review

Cited by 78 publications

References 113 publications

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

Toward Regulatory Effects of Curcumin on Transforming Growth Factor-Beta Across Different Diseases: A Review

Peroxiredoxin-1 Overexpression Attenuates Doxorubicin-Induced Cardiotoxicity by Inhibiting Oxidative Stress and Cardiomyocyte Apoptosis

Natural products and phytochemical nanoformulations targeting mitochondria in oncotherapy: an updated review on resveratrol

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