Selenium unmasks protective iron armor: A possible defense against cutaneous inflammation and cancer

Arbiser, Jack L.; Bonner, Michael Y.; Ward, Nicole L.; Elsey, Justin; Rao, Shikha

doi:10.1016/j.bbagen.2018.05.018

Cited by 43 publications

(26 citation statements)

References 75 publications

(68 reference statements)

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“…This provides an experimental basis for human islet transplantation and the treatment of type one diabetes 83 . In addition, ferroptosis has been found to play a regulatory role in the progression of the diseases, such as acute myeloid leukemia 84 , age-related macular degeneration (AMD) 85 , psoriasis 86 , and hemolytic disorders 87 . In addition, the relationship between ferroptosis and inflammation is also a hot research topic.…”

Section: Ferroptosis and Other Diseasesmentioning

confidence: 99%

Ferroptosis: past, present and future

et al. 2020

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Ferroptosis is a new type of cell death that was discovered in recent years and is usually accompanied by a large amount of iron accumulation and lipid peroxidation during the cell death process; the occurrence of ferroptosis is iron-dependent. Ferroptosis-inducing factors can directly or indirectly affect glutathione peroxidase through different pathways, resulting in a decrease in antioxidant capacity and accumulation of lipid reactive oxygen species (ROS) in cells, ultimately leading to oxidative cell death. Recent studies have shown that ferroptosis is closely related to the pathophysiological processes of many diseases, such as tumors, nervous system diseases, ischemia-reperfusion injury, kidney injury, and blood diseases. How to intervene in the occurrence and development of related diseases by regulating cell ferroptosis has become a hotspot and focus of etiological research and treatment, but the functional changes and specific molecular mechanisms of ferroptosis still need to be further explored. This paper systematically summarizes the latest progress in ferroptosis research, with a focus on providing references for further understanding of its pathogenesis and for proposing new targets for the treatment of related diseases. Facts Ferroptosis is a new type of programmed cell death, which occurs with iron dependence. Ferroptosis plays an important regulatory role in the occurrence and development of many diseases, such as tumors, neurological diseases, acute kidney injury, ischemia/reperfusion, etc. Activating or blocking the ferroptosis pathway to alleviate the progression of the disease, which provides a promising therapeutic strategy for many diseases. Open questions What is the relationship between ferroptosis and other types of cell death? Is it synergy or antagonism? Is iron necessary to promote the production of lipid peroxides, or can other substances take the place of iron in ferroptosis? What is the downstream regulation mechanism of iron in ferroptosis? How can ferroptosis promote the development of inflammation?

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Section: Ferroptosis and Other Diseasesmentioning

confidence: 99%

Ferroptosis: past, present and future

et al. 2020

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“…It is characterized by ROS-induced lipid oxidation and iron overload. Recent findings have suggested that ferroptosis is involved in the pathogenesis of psoriasis, skin cancers, and collagen diseases [ 38 , 39 , 40 ].…”

Section: Roles Of Ros Generated In Skinmentioning

confidence: 99%

What Are Reactive Oxygen Species, Free Radicals, and Oxidative Stress in Skin Diseases?

Nakai

Tsuruta

2021

IJMS

172

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Oxygen in the atmosphere is a crucial component for life-sustaining aerobic respiration in humans. Approximately 95% of oxygen is consumed as energy and ultimately becomes water; however, the remaining 5% produces metabolites called activated oxygen or reactive oxygen species (ROS), which are extremely reactive. Skin, the largest organ in the human body, is exposed to air pollutants, including diesel exhaust fumes, ultraviolet rays, food, xenobiotics, drugs, and cosmetics, which promote the production of ROS. ROS exacerbate skin aging and inflammation, but also function as regulators of homeostasis in the human body, including epidermal keratinocyte proliferation. Although ROS have been implicated in various skin diseases, the underlying mechanisms have not yet been elucidated. Current knowledge on ROS-related and oxidative stress-related skin diseases from basic research to clinical treatment strategies are discussed herein. This information may be applied to the future treatment of skin diseases through the individual targeting of the ROS generated in each case via their inhibition, capture, or regulation.

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“…carbon monoxide and hydrogen sulfide), TGF-β, formyl-Peptide Receptors, Selenoproteins, Galectin-1, and nucleotides (e.g. adenosine and inosine) , ( Arbiser, Bonner, Ward, Elsey, & Rao, 2018 ; Nelson et al, 2016 ; Wallace, Ianaro, Flannigan, & Cirino, 2015 ). Drugs that stimulate resolution include aspirin, statins, omega-3 fatty acids, annexin A1 and annexin A1-derived peptides, statins, glucocorticoids, diclofenac, α-melanocyte stimulating hormone, erythropoietin, kinase inhibitors, galectins, chemerin, adrenocorticotropic hormone, gaseous mediators (e.g.…”

Section: Therapeutic Approachesmentioning

confidence: 99%

Carcinogenesis: Failure of resolution of inflammation?

Fishbein

Hammock

Serhan

et al. 2021

Pharmacology & Therapeutics

140

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Inflammation in the tumor microenvironment is a hallmark of cancer and is recognized as a key characteristic of carcinogens. However, the failure of resolution of inflammation in cancer is only recently being understood. Products of arachidonic acid and related fatty acid metabolism called eicosanoids, including prostaglandins, leukotrienes, lipoxins, and epoxyeicosanoids, critically regulate inflammation, as well as its resolution. The resolution of inflammation is now appreciated to be an active biochemical process regulated by endogenous specialized pro-resolving lipid autacoid mediators which combat infections and stimulate tissue repair/regeneration. Environmental and chemical human carcinogens, including aflatoxins, asbestos, nitrosamines, alcohol, and tobacco, induce tumor-promoting inflammation and can disrupt the resolution of inflammation contributing to a devastating global cancer burden. While mechanisms of carcinogenesis have focused on genotoxic activity to induce mutations, nongenotoxic mechanisms such as inflammation and oxidative stress promote genotoxicity, proliferation, and mutations. Moreover, carcinogens initiate oxidative stress to synergize with inflammation and DNA damage to fuel a vicious feedback loop of cell death, tissue damage, and carcinogenesis. In contrast, stimulation of resolution of inflammation may prevent carcinogenesis by clearance of cellular debris via macrophage phagocytosis and inhibition of an eicosanoid/cytokine storm of pro-inflammatory mediators. Controlling the host inflammatory response and its resolution in carcinogen-induced cancers will be critical to reducing carcinogen-induced morbidity and mortality. Here we review the recent evidence that stimulation of resolution of inflammation, including pro-resolution lipid mediators and soluble epoxide hydrolase inhibitors, may be a new chemopreventive approach to prevent carcinogen-induced cancer that should be evaluated in humans.

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Selenium unmasks protective iron armor: A possible defense against cutaneous inflammation and cancer

Cited by 43 publications

References 75 publications

Ferroptosis: past, present and future

Ferroptosis: past, present and future

What Are Reactive Oxygen Species, Free Radicals, and Oxidative Stress in Skin Diseases?

Carcinogenesis: Failure of resolution of inflammation?

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