Tag: ferroptosis

Nrf2 and Ferroptosis: A New Research Direction for Neurodegenerative Diseases

This review highlights the emerging role of the transcription factor Nrf2 in regulating ferroptosis—a form of programmed cell death driven by iron-dependent lipid peroxidation—within neurodegenerative disease contexts. Ferroptosis contributes to neuronal cell loss in disorders such as Alzheimer’s, Parkinson’s, and Huntington’s diseases. Nrf2 modulates antioxidant defense systems (e.g., glutathione metabolism,

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Ironing out the role of ferroptosis in immunity

This 2024 review article delves into the intricate relationship between ferroptosis—a regulated, iron-dependent form of cell death—and the immune system. It highlights how ferroptosis influences both innate and adaptive immunity, affecting processes such as infection response, autoimmunity, and tumor immunity. The review discusses the dual role of ferroptosis in promoting

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Supraphysiologic Testosterone Induces Ferroptosis and Activates Immune Pathways through Nucleophagy in Prostate Cancer

This 2021 mechanistic study explores how supraphysiologic testosterone (SupraT) affects prostate cancer cells by initiating autophagy-driven processes. SupraT triggers ferritinophagy and nucleophagy, resulting in ferroptosis and degradation of damaged DNA. These mechanisms stimulate cytoplasmic nucleic acid sensors and activate NF-κB signaling, leading to increased secretion of chemokines and cytokines and

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Salinomycin: A new paradigm in cancer therapy

This comprehensive review discusses salinomycin, a polyether antibiotic identified as a potent agent against cancer stem cells (CSCs) and multidrug-resistant tumors. Salinomycin functions by disrupting key oncogenic signaling pathways including Wnt/β-catenin, Notch, Hedgehog, and Akt, reducing CSC viability and enhancing sensitivity to standard chemotherapeutics. Mechanistically, it induces apoptosis, autophagy, and

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Iron: The Cancer Connection

This 2020 review article explores the multifaceted role of iron in cancer biology. It discusses how dysregulated iron metabolism contributes to tumor initiation, growth, and metastasis. Excess iron can promote oxidative DNA damage and genomic instability, facilitating oncogenesis. The article also examines therapeutic strategies targeting iron metabolism, such as iron

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