Redox lipid reprogramming commands susceptibility of macrophages and microglia to ferroptotic death

Kapralov, Alexandr A.; Yang, Qin; Dar, Haider H.; Tyurina, Yulia Y.; Anthonymuthu, Tamil S.; Kim, Rina; Croix, Claudette M. St.; Mikulska-Ruminska, Karolina; Liu, Bing; Shrivastava, Indira H.; Tyurin, Vladimir A.; Ting, Hsiu-Chi; Wu, Yijen; Gao, Yuan; Shurin, Galina V.; Artyukhova, Margarita A; Ponomareva, L. A.; Timashev, Peter; Domingues, Rosário; Stoyanovsky, Detcho A.; Greenberger, Joel S.; Mallampalli, Rama K.; Bahar, İvet; Gabrilovich, Dmitry I.; Bayır, Hülya; Kagan, Valerian E.

doi:10.1038/s41589-019-0462-8

Cited by 385 publications

(302 citation statements)

References 58 publications

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“…112 Ferroptosis also occurs in macrophages. [113][114][115] However, compared with cancer cells, macrophages exert higher resistance to ferroptosis. Erastin and deleting SLC7A11 expression were not sufficient to induce macrophage ferroptosis unless under high iron conditions.…”

Section: The Interaction Of Ferroptosis and Lipid Metabolism Modulatementioning

confidence: 99%

The interaction between ferroptosis and lipid metabolism in cancer

2020

Sig Transduct Target Ther

402

285

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Ferroptosis is a new form of programmed cell death characterized by the accumulation of iron-dependent lethal lipid peroxides. Recent discoveries have focused on alterations that occur in lipid metabolism during ferroptosis and have provided intriguing insights into the interplay between ferroptosis and lipid metabolism in cancer. Their interaction regulates the initiation, development, metastasis, therapy resistance of cancer, as well as the tumor immunity, which offers several potential strategies for cancer treatment. This review is a brief overview of the features characterizing the interaction between ferroptosis and lipid metabolism, and highlights the significance of this interaction in cancer.

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Section: The Interaction Of Ferroptosis and Lipid Metabolism Modulatementioning

confidence: 99%

The interaction between ferroptosis and lipid metabolism in cancer

2020

Sig Transduct Target Ther

402

285

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“…Another study reported that M1 phagocytes exert higher ferroptosis resistance than M2 phagocytes, but that inducible nitric oxide synthase (iNOS)/NO-enrichment of phagocytes can modulate the sensibility of phagocytes to ferroptosis. iNOS depletion/inactivation makes M1 cells sensitive to ferroptosis, while NO donors promote ferroptosis resistance of M2 cells (117). Combining immunotherapy with irradiation can even reverse the chemo-resistance of cancer cells.…”

Section: Clinical Application Of Ferroptosis In Immunotherapymentioning

confidence: 99%

Ferroptosis in Cancer Treatment: Another Way to Rome

Luo

et al. 2020

Front. Oncol.

122

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Ferroptosis is a newly described type of programmed cell death and intensively related to both maintaining homeostasis and the development of diseases, especially cancers. Inducing ferroptosis leads to mitochondrial dysfunction and toxic lipid peroxidation in cells, which plays a pivotal role in suppressing cancer growth and progression. Here, we reviewed the existing studies about the molecular mechanisms of ferroptosis involved in different antitumor treatments, such as chemotherapy, targeted therapy, radiotherapy, and immunotherapy. We focused in particular on the distinct combinatorial therapeutic effects such as the synergistic sensitization effect and the drug-resistance reversal achieved when using ferroptosis inducers with conventional cancer therapy. Finally, we discussed the challenges and opportunities in clinical applications of ferroptosis. The application of nanotechnolgy and other novel technologies may provide a new direction in ferroptosis-driven cancer therapies.

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“…Lastly, it is worth mentioning that NO is a potent inhibitor of lipid peroxidation, and therefore, it is expected to inhibit ferroptosis. Indeed, the antiferroptotic action of NO has recently been demonstrated [119].…”

Section: Ferroptosismentioning

confidence: 99%

Oxidants, Antioxidants and Thiol Redox Switches in the Control of Regulated Cell Death Pathways

Benhar

2020

Antioxidants

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It is well appreciated that biological reactive oxygen and nitrogen species such as hydrogen peroxide, superoxide and nitric oxide, as well as endogenous antioxidant systems, are important modulators of cell survival and death in diverse organisms and cell types. In addition, oxidative stress, nitrosative stress and dysregulated cell death are implicated in a wide variety of pathological conditions, including cancer, cardiovascular and neurological diseases. Therefore, much effort is devoted to elucidate the molecular mechanisms linking oxidant/antioxidant systems and cell death pathways. This review is focused on thiol redox modifications as a major mechanism by which oxidants and antioxidants influence specific regulated cell death pathways in mammalian cells. Growing evidence indicates that redox modifications of cysteine residues in proteins are involved in the regulation of multiple cell death modalities, including apoptosis, necroptosis and pyroptosis. In addition, recent research suggests that thiol redox switches play a role in the crosstalk between apoptotic and necrotic forms of regulated cell death. Thus, thiol-based redox circuits provide an additional layer of control that determines when and how cells die.

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Redox lipid reprogramming commands susceptibility of macrophages and microglia to ferroptotic death

Cited by 385 publications

References 58 publications

The interaction between ferroptosis and lipid metabolism in cancer

The interaction between ferroptosis and lipid metabolism in cancer

Ferroptosis in Cancer Treatment: Another Way to Rome

Oxidants, Antioxidants and Thiol Redox Switches in the Control of Regulated Cell Death Pathways

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