TIGAR alleviates oxidative stress in brain with extended ischemia via a pentose phosphate pathway-independent manner

Liu, Mengru; Zhou, Xinyu; Li, Yue; Ma, Shijia; Pan, Ling; Zhang, Xingxian; Zheng, Wanqing; Wu, Zhenxing; Wang, Ke; Ahsan, Anil; Wu, Jiaying; Jiang, Lei; Lü, Yangyang; Qin, Zheng‐Hong; Chen, Zhong; Zhang, Xiangnan

doi:10.1016/j.redox.2022.102323

Cited by 27 publications

(14 citation statements)

References 43 publications

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“…They further explored the related mechanisms, and found that TIGAR can reduce the expression of Keap1 in OGD-treated neurons, leading to an increase in Nrf2 expression and promoting nuclear translocation. Autophagy inhibitors can inhibit the nuclear translocation of Nrf2 and reduce the expression of Nrf2 target genes, suggesting that autophagy plays antioxidant and neuroprotective roles by activating Nrf2 [ 166 ]. Qi et al found that (±)-5-bromo-2-(5-fluoro-1-hydroxyamyl) benzoate (BFB) promotes the nuclear translocation of Nrf2 by increasing related factors of the p62-Keap1-Nrf2 signaling pathway and confronts the oxidative stress injury induced by hydrogen peroxide in PC12 cells [ 167 ].…”

Section: Crosstalk Between Nrf2 and Autophagy In Ischemic Cerebrovasc...mentioning

confidence: 99%

Nrf2 Pathway and Autophagy Crosstalk: New Insights into Therapeutic Strategies for Ischemic Cerebral Vascular Diseases

Luo

Zheng

2022

Antioxidants

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Cerebrovascular disease is highly prevalent and has a complex etiology and variable pathophysiological activities. It thus poses a serious threat to human life and health. Currently, pathophysiological research on cerebrovascular diseases is gradually improving, and oxidative stress and autophagy have been identified as important pathophysiological activities that are gradually attracting increasing attention. Many studies have found some effects of oxidative stress and autophagy on cerebrovascular diseases, and studies on the crosstalk between the two in cerebrovascular diseases have made modest progress. However, further, more detailed studies are needed to determine the specific mechanisms. This review discusses nuclear factor erythroid 2-related factor 2 (Nrf2) molecules, which are closely associated with oxidative stress and autophagy, and the crosstalk between them, with the aim of providing clues for studying the two important pathophysiological changes and their crosstalk in cerebrovascular diseases as well as exploring new target treatments.

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Section: Crosstalk Between Nrf2 and Autophagy In Ischemic Cerebrovasc...mentioning

confidence: 99%

Nrf2 Pathway and Autophagy Crosstalk: New Insights into Therapeutic Strategies for Ischemic Cerebral Vascular Diseases

Luo

Zheng

2022

Antioxidants

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“…We digested and washed the glioma cells with phosphate-buffered saline (PBS) three times before incubating them with 2,7-dichloro uorescin diacetate (H2DCFDA) at 37 °C for 30 min in the dark. ROS levels in the cells were measured by ow cytometry, according to the manufacturer's instructions [20].…”

Section: Lipid Ros Measurement Assaymentioning

confidence: 99%

Linc01060 suppresses ferroptosis by downregulating SPOP-mediated c-Myc degradation in glioma

Wang

Jiang

et al. 2022

Preprint

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Background: Ferroptosis is a type of regulated cell death induced by iron-dependent lipid peroxidation that plays an essential role in the pathogenesis of various diseases, including cancer. Previously, we reported that long non-coding RNA (lncRNA) Linc01060 regulates aggressive phenotype and aerobic glycolysis in glioma cells. However, the precise functions and underlying molecular mechanisms of Linc01060 in ferroptosis remain unknown.Methods: We explored the upstream regulatory mechanism of Linc01060 expression in hypoxic conditions in glioma cells. The expression and prognostic significance of Linc01060 in patients with glioma was analyzed using data from the Cancer Genome Atlas. The role of Linc01060 in regulating ferroptosis in glioma was evaluated both in vitro and in vivo. Linc01060 expression in clinical glioma specimens was evaluated by fluorescence in situ hybridization, immunofluorescence, and immunohistochemistry.Results: Linc01060 expression was found to be transactivated by hypoxia inducible factor-1 alpha. A strong correlation was found between Linc01060 expression and ferroptosis biomarkers, suggesting that Linc01060 is a negative regulator of ferroptosis. Linc01060 rescued erastin-induced ferroptosis and promoted tumor progression in glioma cells both in vitro and in vivo. Speckle-type POZ protein (SPOP), an E3 ligase of c-Myc, was identified as the target protein of Linc01060. We found that mechanistically Linc01060 competitively binds to SPOP, downregulating SPOP-mediated c-Myc degradation, and thereby decreasing the sensitivity of glioma cells to ferroptosis.Conclusion: Linc01060 suppresses ferroptosis by modulating the SPOP/c-Myc axis in glioma cells. Our results suggest that targeting Linc01060 is a potential strategy for the treatment of tumors.

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“…Glioma cells were digested and washed three times with phosphate-buffered saline (PBS) before incubation with 2,7dichloro uorescin diacetate (H2DCFDA) at 37 °C for 30 min in the dark. ROS levels in the cells were measured using ow cytometry, according to the manufacturer's instructions [33].…”

Section: Lipid Ros Measurement Assaymentioning

confidence: 99%

OMA1 maintains the stemness of glioma stem cells by inducing mitochondrial fission/fusion imbalance

Xiong

Zhu

et al. 2022

Preprint

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Background: Cancer stem cells (CSCs) are the main cause of tumorigenesis, recurrence, and drug resistance and ultimately result in poor clinical outcomes. An imbalance in mitochondrial dynamics is an important manifestation of tumorigenesis. Based on increasing evidence, excessive fission and reduced fusion are common features of many tumors. However, the precise functions and underlying molecular mechanisms of OMA1 in the regulation of mitochondrial homeostasis for CSCs remain unknown. Methods: High-throughput sequencing and bioinformatics were used to select the target molecule, OMA1, and the expression and prognostic significance of OMA1 were analyzed in patients with glioma using data from The Cancer Genome Atlas. The role of OMA1 in regulating mitophagy in gliomas was evaluated in vitro and in vivo. OMA1 expression in clinical glioma specimens was evaluated using western blotting and immunohistochemistry. Results: Glioma stem cells had higher OMA1 expression and distinct mitochondrial morphology than differentiated tumor cells. OMA1 mediated mitochondrial fission, induced mitophagy in tumor cells, and promoted glioma stem cell stemness maintenance via mitophagy. Interestingly, glioma stem cells displayed a unique oxidative phosphorylation dependence. OMA1 promoted tumor progression in glioma cells in vitro and in vivo. Mechanistically, OMA1 promoted mitophagy and maintained Pink1 stability through the Pink1/Parkin signaling pathway. Finally, OMA1 promoted tumor immune escape by upregulating PD-L1 expression. Conclusion: OMA1 promotes phenotype maintenance of glioma stem cells by regulating oxidative phosphorylation homeostasis through the Pink1-Parkin-ROS axis. Overall, OMA1 may be beneficial as a therapeutic strategy for gliomas.

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TIGAR alleviates oxidative stress in brain with extended ischemia via a pentose phosphate pathway-independent manner

Cited by 27 publications

References 43 publications

Nrf2 Pathway and Autophagy Crosstalk: New Insights into Therapeutic Strategies for Ischemic Cerebral Vascular Diseases

Nrf2 Pathway and Autophagy Crosstalk: New Insights into Therapeutic Strategies for Ischemic Cerebral Vascular Diseases

Linc01060 suppresses ferroptosis by downregulating SPOP-mediated c-Myc degradation in glioma

OMA1 maintains the stemness of glioma stem cells by inducing mitochondrial fission/fusion imbalance

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