Heat stress induces ferroptosis-like cell death in plants

Distefano, Ayelén Mariana; Martin, María Victoria; Córdoba, Juan Pablo; Bellido, Andrés Martín; D‘Ippólito, Sebastián; Colman, Silvana Lorena; Soto, Débora; Roldán, Juan Alfredo; Bártoli, Carlos Guillermo; Zabaleta, Eduardo; Fiol, Diego Fernando; Stockwell, Brent R.; Dixon, Scott J.; Pagnussat, Gabriela Carolina

doi:10.1083/jcb.201605110

Cited by 182 publications

(222 citation statements)

References 72 publications

(114 reference statements)

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“…Thus, selenium supplementation promotes ferroptosis resistance, while selenium depletion promotes ferroptosis sensitivity, presumably by modulating GPX4 abundance and activity (Cardoso et al, 2017). A number of other genes have been implicated as modulators of sensitivity to ferroptosis or markers of ferroptosis in diverse contexts: SAT1 , which lies downstream of p53 (Ou et al, 2016) is involved in polyamine metabolism; kiss of death (KOD) in Arabidopsis (Distefano et al, 2017) and FANCD2 in bone marrow stromal cells are induced during ferroptosis (Song et al, 2016); TTC35 , CS , ATP5G3 , and RPL8 are involved in diverse processes in human cancer cells and suppress erastin-induced ferroptosis upon knockdown (Dixon et al, 2012). …”

Section: The Biochemical Control Of Ferroptosismentioning

confidence: 99%

“…Some primary cell systems have also been used for studies of ferroptosis, including HRPTEpiCs (primary human renal proximal tubule epithelial cells), HK2 cells, mouse lung epithelial cells, human bronchial epithelial cells, and spinal motor neurons. In addition, Arabidopsis seedlings exposed to 55 °C heat stress have been used as a model for ferroptotic-like cell death in plants (Distefano et al, 2017). …”

Section: Model Systems In Which Ferroptosis Has Been Observedmentioning

confidence: 99%

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Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

Stockwell

Angeli

Bayır

et al. 2017

Cell

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Summary Ferroptosis is a form of regulated cell death characterized by the iron-dependent accumulation of lipid hydroperoxides to lethal levels. Emerging evidence suggests that ferroptosis represents an ancient vulnerability caused by the incorporation of polyunsaturated fatty acids into cellular membranes, and that cells have developed complex systems that exploit and defend against this vulnerability in different contexts. The sensitivity to ferroptosis is tightly linked to numerous biological processes, including amino acid, iron and polyunsaturated fatty acid metabolism, and the biosynthesis of glutathione, phospholipids, NADPH and coenzyme Q10. Ferroptosis has been implicated in the pathological cell death associated with degenerative diseases (i.e., Alzheimer's, Huntington's, and Parkinson's diseases), carcinogenesis, stroke, intracerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and kidney degeneration in mammals and is also implicated in heat stress in plants. Ferroptosis may also have a tumor suppressor function that could be harnessed for cancer therapy. This Primer reviews the mechanisms underlying ferroptosis, highlights connections to other areas of biology and medicine, and recommends tools and guidelines for studying this emerging form of regulated cell death.

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Section: The Biochemical Control Of Ferroptosismentioning

confidence: 99%

Section: Model Systems In Which Ferroptosis Has Been Observedmentioning

confidence: 99%

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

Stockwell

Angeli

Bayır

et al. 2017

Cell

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4,722

4,352

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“…, desferrioxamine mesylate and deferoxamine). [8] In addition, GPX4, [7,9] heat shock protein beta-1 (HSPB1), [10] and nuclear factor erythroid 2-related factor 2 (Nrf2) function as negative regulators of ferroptosis by limiting ROS production and reducing cellular iron uptake. [8] Previous studies indicate that ferroptosis depends on Ras-ERK signaling and can be completely blocked by MEK inhibition.…”

Section: Introductionmentioning

confidence: 99%

Emerging Strategies of Cancer Therapy Based on Ferroptosis

et al. 2018

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Ferroptosis, a new form of regulated cell death that is iron- and reactive oxygen species dependent, has attracted much attention in the research communities of biochemistry, oncology, and especially material sciences. Since the first demonstration in 2012, a series of strategies have been developed to induce ferroptosis of cancer cells, including the use of nanomaterials, clinical drugs, experimental compounds, and genes. A plethora of research work has outlined the blueprint of ferroptosis as a new option for cancer therapy. However, the published ferroptosis-related reviews have mainly focused on the mechanisms and pathways of ferroptosis, which motivated this contribution to bridge the gap between biological significance and material design. Therefore, it is timely to summarize the previous efforts on the emerging strategies for inducing ferroptosis and shed light on future directions for using such a tool to fight against cancer. Here, the current strategies of cancer therapy based on ferroptosis will be elaborated, the design considerations and the advantages and limitations are highlighted, and finally a future perspective on this emerging field is given.

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“…Different types of RCD have been described in eukaryotes (Melino et al, 2005;Minina et al, 2013). Among them, ferroptosis was recently reported as an oxidative, iron-dependent form of RCD associated with lipid peroxidation and ROS accumulation present in animals, plants and protozoan parasites (Bogacz and Krauth-Siegel, 2018;Conrad et al, 2018;Dangol et al, 2018;Distéfano et al, 2017;Dixon et al, 2012;Stockwell et al, 2017).…”

Section: Introductionmentioning

confidence: 99%

Heat stress induces ferroptosis in a photosynthetic prokaryote

Aguilera

Berdun

Bártoli

et al. 2019

Preprint

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Aguilera et al, show that ferroptosis, an oxidative and iron-dependent form of regulated cell death, plays an important role in the cyanobacterium Synechocystis sp.PCC 6803 in response to heat stress. AbstractFerroptosis is an oxidative and iron-dependent form of regulated cell death (RCD) recently described in eukaryotic organisms like animals, plants and parasites.Here we report that a similar process takes place in the photosynthetic prokaryote Synechocystis sp. PCC 6803 in response to heat stress. After a heat shock, Synechocystis PCC 6803 cells undergo a cell death pathway that can be suppressed by the canonical ferroptosis inhibitors, CPX or Fer-1, or by external addition of calcium (Ca ++ ), glutathione (GSH) or ascorbic acid (AsA). Moreover, as described for eukaryotic cells ferroptosis, this pathway is characterized by an early depletion of the antioxidants GSH and AsA, and by lipid peroxidation. In general, prokaryotes membranes contain poorly oxidizable saturated or monounsaturated lipid molecules, it was thought that free prokaryotes were not susceptible to ferroptosis but interestingly, that is not the case of cyanobacteria, which contain thylakoid membranes that are enriched in polyunsaturated-fatty-acid-containing phospholipids. These results indicate that all of the hallmarks described for eukaryotic ferroptosis are conserved in photosynthetic prokaryotes and suggest that ferroptosis might be an ancient cell death program.

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Heat stress induces ferroptosis-like cell death in plants

Abstract: Distéfano et al. show that an iron-dependent, oxidative cell death process with biochemical and morphological similarities to ferroptosis, as described in mammalian cells, has a physiological role in plants, regulating plant cell death in response to heat stress.

Cited by 182 publications

References 72 publications

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

Emerging Strategies of Cancer Therapy Based on Ferroptosis

Heat stress induces ferroptosis in a photosynthetic prokaryote

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