1,25(OH)2D3 Inhibited Ferroptosis in Zebrafish Liver Cells (ZFL) by Regulating Keap1-Nrf2-GPx4 and NF-κB-hepcidin Axis

Cheng, Ke; Huang, Yanqing; Wang, Chunfang

doi:10.3390/ijms222111334

Cited by 50 publications

(28 citation statements)

References 58 publications

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“…. Cheng et al showed that vitamin D inhibited ferroptosis by activating the Nrf2/GPX4 pathway in zebrafish liver cells ( Cheng et al, 2021 ). Hu et al also demonstrated that vitamin D receptor activation attenuated cisplatin-induced AKI by inhibiting renal tubular epithelial cells ferroptosis via targeting GPX4 ( Hu et al, 2020 ).…”

Section: Treatment Of Aki By Targeting Ferroptosismentioning

confidence: 99%

Ferroptosis and Acute Kidney Injury (AKI): Molecular Mechanisms and Therapeutic Potentials

Feng

Qiao

et al. 2022

Front. Pharmacol.

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Acute kidney injury (AKI), a common and serious clinical kidney syndrome with high incidence and mortality, is caused by multiple pathogenic factors, such as ischemia, nephrotoxic drugs, oxidative stress, inflammation, and urinary tract obstruction. Cell death, which is divided into several types, is critical for normal growth and development and maintaining dynamic balance. Ferroptosis, an iron-dependent nonapoptotic type of cell death, is characterized by iron overload, reactive oxygen species accumulation, and lipid peroxidation. Recently, growing evidence demonstrated the important role of ferroptosis in the development of various kidney diseases, including renal clear cell carcinoma, diabetic nephropathy, and AKI. However, the exact mechanism of ferroptosis participating in the initiation and progression of AKI has not been fully revealed. Herein, we aim to systematically discuss the definition of ferroptosis, the associated mechanisms and key regulators, and pharmacological progress and summarize the most recent discoveries about the role and mechanism of ferroptosis in AKI development. We further conclude its potential therapeutic strategies in AKI.

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Section: Treatment Of Aki By Targeting Ferroptosismentioning

confidence: 99%

Ferroptosis and Acute Kidney Injury (AKI): Molecular Mechanisms and Therapeutic Potentials

Feng

Qiao

et al. 2022

Front. Pharmacol.

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“…There is also a suggested inverse relationship between the risk for developing endometriosis and plasma levels of 25-hydroxyvitamin D [25(OH 2 )D] [ 125 ]. One other mechanism through which vitamin D may reduce oxidative stress is through its iron regulatory function as it acts on hepcidin and ferroportin which are involved in the intestinal absorption of iron [ 118 , 126 ]. Activation and downstream signaling of the vitamin D receptor (VDR) has also been implicated in the inhibition of ferroptosis by regulating the expression of GPX4 and by reducing lipid peroxidation [ 127 ].…”

Section: Treatments For Oxidative Stressmentioning

confidence: 99%

Targeting Oxidative Stress Involved in Endometriosis and Its Pain

et al. 2022

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Endometriosis is a common gynecological disorder seen in women and is characterized by chronic pelvic pain and infertility. This disorder is becoming more prevalent with increased morbidity. The etiology of endometriosis remains to be fully elucidated, which will lead to improved therapeutic options. In this review, we will evaluate the biochemical mechanisms leading to oxidative stress and their implication in the pathophysiology of endometriosis, as well as potential treatments that target these processes. A comprehensive exploration of previous research revealed that endometriosis is associated with elevated reactive oxygen species and oxidation products, decreased antioxidants and detoxification enzymes, and dysregulated iron metabolism. High levels of oxidative stress contributed to inflammation, extracellular matrix degradation, angiogenesis, and cell proliferation, which may explain its role in endometriosis. Endometriosis-associated pain was attributed to neurogenic inflammation and a feed-forward mechanism involving macrophages, pro-inflammatory cytokines, and pain-inducing prostaglandins. N-acetylcysteine, curcumin, melatonin, and combined vitamin C and E supplementation displayed promising results for the treatment of endometriosis, but further research is needed for their use in this population.

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“…Vitamin D is a fat-soluble vitamin essential for calcium homeostasis and is produced by ultraviolet light in the dermis or epidermis and activated by successive 25- and 1-hydroxylations in the liver and kidney, respectively ( 83 ). 1,25-dihydroxyvitanmin D was shown to protect zebrafish liver cells from ferroptosis, concomitant with decreases in hepcidin expression and cellular iron contents ( 84 ). Moreover, it was demonstrated that vitamin D receptor activation inhibits ferroptotic cell death in human renal proximal tubule cells and mouse hippocampal cells ( 85 , 86 ).…”

Section: Prevention Of Iron-induced Liver Damage By Nutrientsmentioning

confidence: 99%

Iron-Induced Hepatocarcinogenesis—Preventive Effects of Nutrients

Tsuchiya

2022

Front. Oncol.

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The liver is a primary organ that stores body iron, and plays a central role in the regulation of iron homeostasis. Hepatic iron overload (HIO) is a prevalent feature among patients with chronic liver diseases (CLDs), including alcoholic/nonalcoholic liver diseases and hepatitis C. HIO is suggested to promote the progression toward hepatocellular carcinoma because of the pro-oxidant nature of iron. Iron metabolism is tightly regulated by various factors, such as hepcidin and ferroportin, in healthy individuals to protect the liver from such deteriorative effects. However, their intrinsic expressions or functions are frequently compromised in patients with HIO. Thus, various nutrients have been reported to regulate hepatic iron metabolism and protect the liver from iron-induced damage. These nutrients are beneficial in HIO-associated CLD treatment and eventually prevent iron-mediated hepatocarcinogenesis. This mini-review aimed to discuss the mechanisms and hepatocarcinogenic risk of HIO in patients with CLDs. Moreover, nutrients that hold the potential to prevent iron-induced hepatocarcinogenesis are summarized.

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1,25(OH)2D3 Inhibited Ferroptosis in Zebrafish Liver Cells (ZFL) by Regulating Keap1-Nrf2-GPx4 and NF-κB-hepcidin Axis

Cited by 50 publications

References 58 publications

Ferroptosis and Acute Kidney Injury (AKI): Molecular Mechanisms and Therapeutic Potentials

Ferroptosis and Acute Kidney Injury (AKI): Molecular Mechanisms and Therapeutic Potentials

Targeting Oxidative Stress Involved in Endometriosis and Its Pain

Iron-Induced Hepatocarcinogenesis—Preventive Effects of Nutrients

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