Posttranslational Modifications in Ferroptosis

Wei, Xiang; Yi, Xin; Zhu, Xiashi; Jiang, Ding-Sheng

doi:10.1155/2020/8832043

Cited by 131 publications

(96 citation statements)

References 113 publications

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“…Some pharmacotherapies, such as metformin [ 191 ] and galangin [ 192 ], suppress ferroptosis and exert cerebroprotective effects in the context of CIRI by decreasing lipid peroxidation production or increasing the expression of GPX4. Apart from that efficacy, metformin (1,1-Dimethylbiguanide), a hypoglycemic drug, leads to glucose starvation which results in the phosphorylation and activation of adenosine 5′-monophosphate-activated protein kinase (AMPK) [ 193 , 194 ]. This kinase suppresses PUFA-containing lipid biosynthesis and then inhibits ferroptosis [ 194 , 195 ].…”

Section: Pharmacotherapies Against Ciri Targeting Ferroptosis and Necroptosismentioning

confidence: 99%

“…Apart from that efficacy, metformin (1,1-Dimethylbiguanide), a hypoglycemic drug, leads to glucose starvation which results in the phosphorylation and activation of adenosine 5′-monophosphate-activated protein kinase (AMPK) [ 193 , 194 ]. This kinase suppresses PUFA-containing lipid biosynthesis and then inhibits ferroptosis [ 194 , 195 ]. In addition to galangin, the therapeutics of other Chinese herbs and their bioactive constituents against CIRI cannot be ignored.…”

Section: Pharmacotherapies Against Ciri Targeting Ferroptosis and Necroptosismentioning

confidence: 99%

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Insight into Crosstalk between Ferroptosis and Necroptosis: Novel Therapeutics in Ischemic Stroke

Zhou

Liao

Mei

et al. 2021

Oxidative Medicine and Cellular Longevity

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Ferroptosis is a nonapoptotic form of cell death characterized by iron-dependent accumulation of lipid hydroperoxides to lethal levels. Necroptosis, an alternative form of programmed necrosis, is regulated by receptor-interacting protein (RIP) 1 activation and by RIP3 and mixed-lineage kinase domain-like (MLKL) phosphorylation. Ferroptosis and necroptosis both play important roles in the pathological progress in ischemic stroke, which is a complex brain disease regulated by several cell death pathways. In the past few years, increasing evidence has suggested that the crosstalk occurs between necroptosis and ferroptosis in ischemic stroke. However, the potential links between ferroptosis and necroptosis in ischemic stroke have not been elucidated yet. Hence, in this review, we overview and analyze the mechanism underlying the crosstalk between necroptosis and ferroptosis in ischemic stroke. And we find that iron overload, one mechanism of ferroptosis, leads to mitochondrial permeability transition pore (MPTP) opening, which aggravates RIP1 phosphorylation and contributes to necroptosis. In addition, heat shock protein 90 (HSP90) induces necroptosis and ferroptosis by promoting RIP1 phosphorylation and suppressing glutathione peroxidase 4 (GPX4) activation. In this work, we try to deliver a new perspective in the exploration of novel therapeutic targets for the treatment of ischemic stroke.

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Section: Pharmacotherapies Against Ciri Targeting Ferroptosis and Necroptosismentioning

confidence: 99%

Section: Pharmacotherapies Against Ciri Targeting Ferroptosis and Necroptosismentioning

confidence: 99%

Insight into Crosstalk between Ferroptosis and Necroptosis: Novel Therapeutics in Ischemic Stroke

Zhou

Liao

Mei

et al. 2021

Oxidative Medicine and Cellular Longevity

View full text Add to dashboard Cite

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“…GCH1 is a rate-limiting enzyme for the synthesis of tetrahydrobiopterin. Overexpression of GCH1 can eliminate lipid peroxidation and almost completely inhibit ferroptosis ( Wei et al, 2020 ). In high-grade serous ovarian cancers, due to the silencing of PML , ROS content, lipid peroxidation, and lysosomes, and the lysosomal Fe2 + levels are reduced, which can result in potential ferroptosis and improved sensitivity to immunotherapy ( Gentric et al, 2019 ).…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis-Related Gene Signature Predicts the Prognosis of Skin Cutaneous Melanoma and Response to Immunotherapy

Xie

Mao

et al. 2021

Front. Genet.

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Ferroptosis is a non-apoptotic regulated cell death process, and much research has indicated that ferroptosis can induce the non-apoptotic death of tumor cells. Ferroptosis-related genes are expected to become a biological target for cancer treatment. However, the regulation of ferroptosis-related genes in skin cutaneous melanoma (SKCM) has not been well studied. In the present study, we conducted a systematic analysis of SKCM based on RNA sequencing data and clinical data obtained from The Cancer Genome Atlas (TCGA) database and the FerrD database. SKCM patients from the GSE78220 and MSKCC cohorts were used for external validation. Applying consensus clustering on RNA sequencing data from TCGA the generated ferroptosis subclasses of SKCM, which were analyzed based on the set of differentially expressed ferroptosis-related genes. Then, a least absolute shrinkage and selection operator (LASSO)-Cox regression was used to construct an eight gene survival-related linear signature. The median cut-off risk score was used to divide patients into high- and low-risk groups. The time-dependent receiver operating characteristic curve was used to examine the predictive power of the model. The areas under the curve of the signature at 1, 3, and 5 years were 0.673, 0.716, and 0.746, respectively. Kaplan-Meier survival analysis showed that the prognosis of high-risk patients was worse than that of low-risk patients. Univariate and multivariate Cox regression analyses showed that the risk signature was a robust independent prognostic indicator. By incorporating risk scores with tumor staging, a nomogram was constructed to predict prognostic outcomes for SKCM patients. In addition, the immunological analysis showed different immune cell infiltration patterns. Programmed-death-1 (PD-1) immunotherapy showed more significant benefits in the low-risk group than in the high-risk group. In summary, a model based on ferroptosis-related genes can predict the prognosis of SKCM and could have a potential role in guiding targeted therapy of SKCM.

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“…Administration of folate or its metabolic precursor BH4 was evidenced to relieve colitis-related tissue damage, detrimental inflammation, and malignant tumorigenesis [ 138 , 139 ]. GCH1-mediated BH4 biosynthesis is crucial for ferroptosis resistance by remodeling lipidomic composition and suppressing lipid peroxidation [ 67 , 140 ]. Ionizing radiation decreases BH4 levels and increases superoxide anion accumulation in patients and rats after radiotherapy due to the downregulation of GCH1.…”

Section: Ferroptosis and Inflammatory Bowel Diseasementioning

confidence: 99%

Emerging Pathological Engagement of Ferroptosis in Gut Diseases

Gao

Zhang

2021

Oxidative Medicine and Cellular Longevity

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Inflammatory bowel disease (IBD), including ulcerative colitis and Crohn’s disease, is mainly characterized by chronic and progressive inflammation that damages the gastrointestinal mucosa. Increasing studies have enlightened that dysregulated cell death occurs in the inflamed sites, leading to the disruption of the intestinal barrier and aggravating inflammatory response. Ferroptosis, a newly characterized form of regulated cell death, is driven by the lethal accumulation of lipid peroxides catalyzed by cellular free iron. It has been widely documented that the fundamental features of ferroptosis, including iron deposition, GSH exhaustion, GPX4 inactivation, and lipid peroxidation, are manifested in the injured gastrointestinal tract in IBD patients. Furthermore, manipulation of the critical ferroptotic genes could alter the progression, severity, or even morbidity of the experimental colitis. Herein, we critically summarize the recent advances in the field of ferroptosis, focusing on interpreting the potential engagement of ferroptosis in the pathogenesis of IBD. Moreover, we are attempting to shed light on a perspective insight into the possibility of targeting ferroptosis as novel therapeutic designs for the clinical intervention of these gastrointestinal diseases.

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Posttranslational Modifications in Ferroptosis

Cited by 131 publications

References 113 publications

Insight into Crosstalk between Ferroptosis and Necroptosis: Novel Therapeutics in Ischemic Stroke

Insight into Crosstalk between Ferroptosis and Necroptosis: Novel Therapeutics in Ischemic Stroke

Ferroptosis-Related Gene Signature Predicts the Prognosis of Skin Cutaneous Melanoma and Response to Immunotherapy

Emerging Pathological Engagement of Ferroptosis in Gut Diseases

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