4.6 Review

Research progress of ferroptosis in glaucoma and optic nerve damage

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Regulatory pathways and drugs associated with ferroptosis in tumors

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Summary: In this article, we reviewed the regulation of ferroptosis in tumor cells and introduced the tumor-related signaling pathways of ferroptosis. Special attention was given to the role of noncoding RNA, nanomaterials, drug effects, and targeted treatment using ferroptosis drugs. The currently unresolved issues and future research directions for ferroptosis in tumor cells were discussed, along with the prospects of this emerging field.

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Tumor suppressor p53 promotes ferroptosis in oxidative stress conditions independent of modulation of ferroptosis by p21, CDKs, RB, and E2F

Nishanth Kuganesan et al.

Summary: The study revealed that p53 enhances ferroptosis while p21 suppresses it. Elevated CDK activity inhibits ferroptosis, and overexpression of E2F partially suppresses ferroptosis through a p21-dependent mechanism. Deletion of RB genes enhances ferroptosis, showing a complex regulation within the p53 tumor suppressor pathway affecting ferroptotic sensitivity.

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Risk Factors for Retinal Ganglion Cell Distress in Glaucoma and Neuroprotective Potential Intervention

Stefania Vernazza et al.

Summary: Glaucoma is a neurodegenerative disease that causes damage to retinal ganglion cells and results in permanent vision loss. While Intra Ocular Pressure (IOP) is the main therapeutic target, other pathological conditions and neuroprotective therapeutic approaches also play important roles in the disease progression.

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Gulgun Tezel

Summary: Glaucoma is a chronic neurodegenerative disease characterized by apoptosis of retinal ganglion cells and degeneration of axons. The disease involves multiple triggers, cell types, and molecular pathways, with both intrinsic responses of RGCs and interactions of surrounding glia playing decisive roles in cell fate. Mitochondrial dysfunction and glia-driven neuroinflammation have widespread impacts in the glaucomatous retina and optic nerve, suggesting potential unified treatment strategies to protect RGCs.
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Iron Accumulation and Lipid Peroxidation in the Aging Retina: Implication of Ferroptosis in Age-Related Macular Degeneration

Tantai Zhao et al.

Summary: Iron is crucial in various biological processes in the human body, playing a critical role in the visual phototransduction cascade in the retina. Excess iron can be toxic and contribute to oxidative stress-induced cell death in the aging retina, predisposing it to conditions like AMD characterized by iron accumulation and lipid peroxidation. Understanding iron accumulation mechanisms and lipid peroxidation, particularly through ferroptosis, is essential for delving into the pathogenesis of cell death and AMD.

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Cysteine depletion induces pancreatic tumor ferroptosis in mice

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The Impact of Iron Overload and Ferroptosis on Reproductive Disorders in Humans: Implications for Preeclampsia

Shu-Wing Ng et al.

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Clockophagy is a novel selective autophagy process favoring ferroptosis

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The relation between dietary intake and glaucoma: a systematic review

Wishal D. Ramdas

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Mitochondrial rescue prevents glutathione peroxidase-dependent ferroptosis

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Tau-mediated iron export prevents ferroptotic damage after ischemic stroke

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Autophagy promotes ferroptosis by degradation of ferritin

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Glutaminolysis and Transferrin Regulate Ferroptosis

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Two independent pathways of regulated necrosis mediate ischemia-reperfusion injury

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