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ferroptosis

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https://www.readbyqxmd.com/read/28525763/principles-of-chemical-biology-from-antibiotic-resistance-to-rna-targeted-therapy-via-autoxidation-and-lipid-droplets
#1
(no author information available yet)
This month: Ribosome mutations and multi-antibiotic resistance, role of autoxidation in ferroptosis, ceramide metabolism, and finding RNA drug targets.
May 18, 2017: Cell Chemical Biology
https://www.readbyqxmd.com/read/28515173/heme-oxygenase-1-mitigates-ferroptosis-in-renal-proximal-tubule-cells
#2
Oreoluwa Adedoyin, Ravindra Boddu, Amie M Traylor, Jeremie M Lever, Subhashini Bolisetty, James George, Anupam Agarwal
Ferroptosis is an iron-dependent form of regulated, non-apoptotic cell death, which contributes to damage in models of acute kidney injury (AKI). Heme oxygenase-1 (HO-1) is a cytoprotective enzyme induced in response to cellular stress, and is protective against AKI due to its anti-apoptotic and anti-inflammatory properties. However, the role of HO-1 in regulating ferroptosis is unclear. The purpose of this study was to elucidate the role of HO-1 in regulating ferroptotic cell death in renal proximal tubule cells (PTCs)...
May 17, 2017: American Journal of Physiology. Renal Physiology
https://www.readbyqxmd.com/read/28494534/ferroptosis-a-novel-anti-tumor-action-for-cisplatin
#3
Jipeng Guo, Bingfei Xu, Qi Han, Hongxia Zhou, Yun Xia, Chongwen Gong, Xiaofang Dai, Zhenyu Li, Gang Wu
Purpose: Ferroptosis is a new mode of regulated cell death, which is completely distinct from other cell death modes based on morphological, biochemical, and genetic criteria. This study evaluated the therapeutic role of ferroptosis in classic chemotherapy drugs, including the underlying mechanism. Materials and Methods: Cell viability was detected by using the Methylthiazoltetrazlium dye uptake method. RNAi was used to knockout iron-responsive element binding protein 2, and PCR, western blot was used to evaluate the efficiency...
May 10, 2017: Cancer Research and Treatment: Official Journal of Korean Cancer Association
https://www.readbyqxmd.com/read/28489094/theoretical-insights-into-the-mechanism-of-ferroptosis-suppression-via-inactivation-of-a-lipid-peroxide-radical-by-liproxstatin-1
#4
Xiehuang Sheng, Chao Shan, Jianbiao Liu, Jintong Yang, Bin Sun, Dezhan Chen
Ferroptosis is a recently discovered iron-dependent form of non-apoptotic cell death caused by the accumulation of membrane lipid peroxidation products, which is involved in various pathological conditions of the brain, kidney, liver and heart. A potent spiroquinoxalinamine derivative named liproxstatin-1 is discovered by high-throughput screening, which is able to suppress ferroptosis via lipid peroxide scavenging in vivo. Thus, molecular simulations, density functional theory (DFT) and variational transition-state theory with a small-curvature tunneling (SCT) coefficient are utilized to elucidate the detailed mechanisms of inactivation of a lipid peroxide radical by liproxstatin-1...
May 10, 2017: Physical Chemistry Chemical Physics: PCCP
https://www.readbyqxmd.com/read/28470518/ferroptosis-and-cell-death-analysis-by-flow-cytometry
#5
Daishi Chen, Ilker Y Eyupoglu, Nicolai Savaskan
Cell death and its recently discovered regulated form ferroptosis are characterized by distinct morphological, electrophysiological, and pharmacological features. In particular ferroptosis can be induced by experimental compounds and clinical drugs (i.e., erastin, sulfasalazine, sorafenib, and artesunate) in various cell types and cancer cells. Pharmacologically, this cell death process can be inhibited by iron chelators and lipid peroxidation inhibitors. Relevance of this specific cell death form has been found in different pathological conditions such as cancer, neurotoxicity, neurodegeneration, and ischemia...
2017: Methods in Molecular Biology
https://www.readbyqxmd.com/read/28462584/gpx4-lipid-peroxidation-and-cell-death-discoveries-rediscoveries-and-open-issues
#6
Matilde Maiorino, Marcus Conrad, Fulvio Ursini
SIGNIFICANCE: Iron-dependent lipid peroxidation is a complex oxidative process where phospholipid hydroperoxides (PLOOH) are produced in membranes and finally transformed into a series of decomposition products, some of which endowed with biological activity. It is specifically prevented by GPx4, the selenoenzyme that reduces PLOOH by glutathione (GSH). PLOOH is both a product and the major initiator of peroxidative chain reactions, as well as an activator of lipoxygenases. -Tocopherol both specifically breaks peroxidative chain propagation and inhibits lipoxygenases...
May 2, 2017: Antioxidants & Redox Signaling
https://www.readbyqxmd.com/read/28462529/ferroptosis-bug-or-feature
#7
REVIEW
Scott J Dixon
Ferroptosis is an iron-dependent, oxidative form of non-apoptotic cell death. This form of cell death does not share morphological, biochemical, or genetic similarities with classic necrosis, necroptosis, parthanatos, or other forms of non-apoptotic cell death. Ferroptosis can be triggered by depleting the cell of the amino acid cysteine, or by inhibiting the phospholipid hydroperoxidase glutathione peroxidase 4 (GPX4). Why certain stimuli trigger ferroptosis instead of another form of cell death, and whether this process could be adaptive in vivo, are two major unanswered questions concerning this process...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28462528/the-in-vivo-evidence-for-regulated-necrosis
#8
REVIEW
Wulf Tonnus, Andreas Linkermann
Necrosis is a hallmark of several widespread diseases or their direct complications. In the past decade, we learned that necrosis can be a regulated process that is potentially druggable. RIPK3- and MLKL-mediated necroptosis represents by far the best studied pathway of regulated necrosis. During necroptosis, the release of damage-associated molecular patterns (DAMPs) drives a phenomenon referred to as necroinflammation, a common consequence of necrosis. However, most studies of regulated necrosis investigated cell lines in vitro in a cell autonomous manner, which represents a non-physiological situation...
May 2017: Immunological Reviews
https://www.readbyqxmd.com/read/28434137/cholesterol-hydroperoxide-generation-translocation-and-reductive-turnover-in-biological-systems
#9
Albert W Girotti, Witold Korytowski
Cholesterol is like other unsaturated lipids in being susceptible to peroxidative degradation upon exposure to strong oxidants like hydroxyl radical or peroxynitrite generated under conditions of oxidative stress. In the eukaryotic cell plasma membrane, where most of the cellular cholesterol resides, peroxidation leads to membrane structural and functional damage from which pathological states may arise. In low density lipoprotein, cholesterol and phospholipid peroxidation have long been associated with atherogenesis...
April 22, 2017: Cell Biochemistry and Biophysics
https://www.readbyqxmd.com/read/28433662/iron-and-thiol-redox-signaling-in-cancer-an-exquisite-balance-to-escape-ferroptosis
#10
REVIEW
Shinya Toyokuni, Fumiya Ito, Kyoko Yamashita, Yasumasa Okazaki, Shinya Akatsuka
Epidemiological data indicate a constant worldwide increase in cancer mortality, although the age of onset is increasing. Recent accumulation of genomic data on human cancer via next-generation sequencing confirmed that cancer is a disease of genome alteration. In many cancers, the Nrf2 transcription system is activated via mutations either in Nrf2 or Keap1 ubiquitin ligase, leading to persistent activation of the genes with antioxidative functions. Furthermore, deep sequencing of passenger mutations is clarifying responsible cancer causative agent(s) in each case, including aging, APOBEC activation, smoking and UV...
April 19, 2017: Free Radical Biology & Medicine
https://www.readbyqxmd.com/read/28405617/inhibition-of-neuronal-ferroptosis-protects-hemorrhagic-brain
#11
Qian Li, Xiaoning Han, Xi Lan, Yufeng Gao, Jieru Wan, Frederick Durham, Tian Cheng, Jie Yang, Zhongyu Wang, Chao Jiang, Mingyao Ying, Raymond C Koehler, Brent R Stockwell, Jian Wang
Intracerebral hemorrhage (ICH) causes high mortality and morbidity, but our knowledge of post-ICH neuronal death and related mechanisms is limited. In this study, we first demonstrated that ferroptosis, a newly identified form of cell death, occurs in the collagenase-induced ICH model in mice. We found that administration of ferrostatin-1, a specific inhibitor of ferroptosis, prevented neuronal death and reduced iron deposition induced by hemoglobin in organotypic hippocampal slice cultures (OHSCs). Mice treated with ferrostatin-1 after ICH exhibited marked brain protection and improved neurologic function...
April 6, 2017: JCI Insight
https://www.readbyqxmd.com/read/28386601/on-the-mechanism-of-cytoprotection-by-ferrostatin-1-and-liproxstatin-1-and-the-role-of-lipid-peroxidation-in-ferroptotic-cell-death
#12
Omkar Zilka, Ron Shah, Bo Li, José Pedro Friedmann Angeli, Markus Griesser, Marcus Conrad, Derek A Pratt
Ferroptosis is a form of regulated necrosis associated with the iron-dependent accumulation of lipid hydroperoxides that may play a key role in the pathogenesis of degenerative diseases in which lipid peroxidation has been implicated. High-throughput screening efforts have identified ferrostatin-1 (Fer-1) and liproxstatin-1 (Lip-1) as potent inhibitors of ferroptosis - an activity that has been ascribed to their ability to slow the accumulation of lipid hydroperoxides. Herein we demonstrate that this activity likely derives from their reactivity as radical-trapping antioxidants (RTAs) rather than their potency as inhibitors of lipoxygenases...
March 22, 2017: ACS Central Science
https://www.readbyqxmd.com/read/28384611/bid-links-ferroptosis-to-mitochondrial-cell-death-pathways
#13
Sandra Neitemeier, Anja Jelinek, Vincenzo Laino, Lena Hoffmann, Ina Eisenbach, Roman Eying, Goutham K Ganjam, Amalia M Dolga, Sina Oppermann, Carsten Culmsee
Ferroptosis has been defined as an oxidative and iron-dependent pathway of regulated cell death that is distinct from caspase-dependent apoptosis and established pathways of death receptor-mediated regulated necrosis. While emerging evidence linked features of ferroptosis induced e.g. by erastin-mediated inhibition of the Xc(-) system or inhibition of glutathione peroxidase 4 (Gpx4) to an increasing number of oxidative cell death paradigms in cancer cells, neurons or kidney cells, the biochemical pathways of oxidative cell death remained largely unclear...
March 9, 2017: Redox Biology
https://www.readbyqxmd.com/read/28367812/-autophagy-and-iron-homeostasis
#14
Ahmed Hamaï, Maryam Mehrpour
Iron is an essential nutrient to life. However, the ability of iron to cycle between the oxidized and reduced forms contributes to the formation of reactive oxygen species. The generation of free radicals leads to oxidative stress and the initiation of signaling pathways involved in cell survival or cell death. The iron homeostasis is very carefully regulated and dysregulation of iron metabolism contributes to various human pathologies. The work carried out in recent years has revealed new cellular processes and mechanisms like ferritinophagy, that deepen our understanding of iron homeostasis...
March 2017: Médecine Sciences: M/S
https://www.readbyqxmd.com/read/28363764/ferroptosis-inhibition-mechanisms-and-opportunities
#15
REVIEW
Jose Pedro Friedmann Angeli, Ron Shah, Derek A Pratt, Marcus Conrad
The past decade has yielded tremendous insights into how cells die. This has come with our understanding that several distinct forms of cell death are encompassed under the umbrella term necrosis. Among these distinct forms of regulated necrotic cell death, ferroptosis has attracted considerable attention owing to its putative involvement in diverse pathophysiological processes. A key feature of the ferroptosis process is the requirement of phospholipid peroxidation, a process that has been linked with several human pathologies...
May 2017: Trends in Pharmacological Sciences
https://www.readbyqxmd.com/read/28362726/-hints-in-the-killer-protein-gasdermin-d-unveiling-the-secrets-of-gasdermins-driving-cell-death
#16
REVIEW
Shiqiao Qiu, Jing Liu, Feiyue Xing
Pyroptosis is a lytic form of cell death distinguished from apoptosis, ferroptosis, necrosis, necroptosis, NETosis, oncosis, pyronecrosis and autophagy. Proinflammatory caspases cleave a gasdermin D (GSDMD) protein to generate a 31 kDa N-terminal domain. The cleavage relieves the intramolecular inhibition on the gasdermin-N domain, which then moves to the plasma membrane to exhibit pore-forming activity. Thus, GSDMD acts as the final and direct executor of pyroptotic cell death. Owing to the selective targeting of the inner leaflet of the plasma membrane with the pore-forming that determines pyroptotic cell death, GSDMD could be a potential target to control cell death or extracellular bacterial infections...
April 2017: Cell Death and Differentiation
https://www.readbyqxmd.com/read/28358377/mitochondrial-complex-i-inhibition-triggers-a-mitophagy-dependent-ros-increase-leading-to-necroptosis-and-ferroptosis-in-melanoma-cells
#17
Farhan Basit, Lisanne Mpe van Oppen, Laura Schöckel, Hasse M Bossenbroek, Sjenet E van Emst-de Vries, Johannes Cw Hermeling, Sander Grefte, Charlotte Kopitz, Melanie Heroult, Peter Hgm Willems, Werner Jh Koopman
Inhibition of complex I (CI) of the mitochondrial respiratory chain by BAY 87-2243 ('BAY') triggers death of BRAF(V600E) melanoma cell lines and inhibits in vivo tumor growth. Here we studied the mechanism by which this inhibition induces melanoma cell death. BAY treatment depolarized the mitochondrial membrane potential (Δψ), increased cellular ROS levels, stimulated lipid peroxidation and reduced glutathione levels. These effects were paralleled by increased opening of the mitochondrial permeability transition pore (mPTP) and stimulation of autophagosome formation and mitophagy...
March 30, 2017: Cell Death & Disease
https://www.readbyqxmd.com/read/28351498/iron-accumulation-glutathione-depletion-and-lipid-peroxidation-must-occur-simultaneously-during-ferroptosis-and-are-mutually-amplifying-events
#18
Robert L Bertrand
Ferroptosis is a recently discovered form of regulated necrosis that involves iron-dependent lipid peroxidation. How cells die once ferroptosis is triggered remains unclear. Ferroptosis is hypothesized to require three critical events: (1) accumulation of redox-active iron, (2) glutathione depletion, and (3) lipid peroxidation. It is proposed that these three events must unfold simultaneously because stopping any critical event also stops ferroptosis. These events are hypothesized to amplify in severity through positive feedback loops...
April 2017: Medical Hypotheses
https://www.readbyqxmd.com/read/28319068/iron-addiction-a-novel-therapeutic-target-in-ovarian-cancer
#19
D Basuli, L Tesfay, Z Deng, B Paul, Y Yamamoto, G Ning, W Xian, F McKeon, M Lynch, C P Crum, P Hegde, M Brewer, X Wang, L D Miller, N Dyment, F M Torti, S V Torti
Ovarian cancer is a lethal malignancy that has not seen a major therapeutic advance in over 30 years. We demonstrate that ovarian cancer exhibits a targetable alteration in iron metabolism. Ferroportin (FPN), the iron efflux pump, is decreased, and transferrin receptor (TFR1), the iron importer, is increased in tumor tissue from patients with high grade but not low grade serous ovarian cancer. A similar profile of decreased FPN and increased TFR1 is observed in a genetic model of ovarian cancer tumor-initiating cells (TICs)...
March 20, 2017: Oncogene
https://www.readbyqxmd.com/read/28297659/oncogene-selective-sensitivity-to-synchronous-cell-death-following-modulation-of-the-amino-acid-nutrient-cystine
#20
Ioannis Poursaitidis, Xiaomeng Wang, Thomas Crighton, Christiaan Labuschagne, David Mason, Shira L Cramer, Kendra Triplett, Rajat Roy, Olivier E Pardo, Michael J Seckl, Scott W Rowlinson, Everett Stone, Richard F Lamb
Cancer cells reprogram their metabolism, altering both uptake and utilization of extracellular nutrients. We individually depleted amino acid nutrients from isogenic cells expressing commonly activated oncogenes to identify correspondences between nutrient supply and viability. In HME (human mammary epithelial) cells, deprivation of cystine led to increased cell death in cells expressing an activated epidermal growth factor receptor (EGFR) mutant. Cell death occurred via synchronous ferroptosis, with generation of reactive oxygen species (ROS)...
March 14, 2017: Cell Reports
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