Melatonin and ferroptosis: Mechanisms and therapeutic implications

Biochemical Pharmacology, Год журнала: 2023, Номер 218, С. 115909 - 115909

Опубликована: Ноя. 4, 2023

Язык: Английский

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Age-related macular degeneration and neurodegenerative disorders: Shared pathways in complex interactions

Survey of Ophthalmology, Год журнала: 2023, Номер 69(3), С. 303 - 310

Опубликована: Ноя. 23, 2023

Язык: Английский

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Upregulation of HMOX1 associated with M2 macrophage infiltration and ferroptosis in proliferative diabetic retinopathy

International Immunopharmacology, Год журнала: 2024, Номер 134, С. 112231 - 112231

Опубликована: Май 12, 2024

Язык: Английский

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Resveratrol Protects Müller Cells Against Ferroptosis in the Early Stage of Diabetic Retinopathy by Regulating the Nrf2/GPx4/PTGS2 Pathway

Molecular Neurobiology, Год журнала: 2024, Номер unknown

Опубликована: Сен. 18, 2024

Язык: Английский

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A highly selective inhibitor of discoidin domain receptor‐1 (DDR1‐IN‐1) protects corneal epithelial cells from YAP/ACSL4‐mediated ferroptosis in dry eye

British Journal of Pharmacology, Год журнала: 2024, Номер 181(21), С. 4245 - 4261

Опубликована: Июль 8, 2024

This study investigated the involvement of discoidin domain receptor (DDR) in dry eye and assessed potential specific DDR inhibitors as a therapeutic strategy for by exploring underlying mechanism.

Язык: Английский

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Role of ferroptosis in mitochondrial damage in diabetic retinopathy

Free Radical Biology and Medicine, Год журнала: 2024, Номер unknown

Опубликована: Окт. 1, 2024

Язык: Английский

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JAG1/Notch Pathway Inhibition Induces Ferroptosis and Promotes Cataractogenesis

International Journal of Molecular Sciences, Год журнала: 2025, Номер 26(1), С. 307 - 307

Опубликована: Янв. 1, 2025

Cataracts remain the leading cause of visual impairment worldwide, yet underlying molecular mechanisms, particularly in age-related cataracts (ARCs), are not fully understood. The Notch signaling pathway, known for its critical role various degenerative diseases, may also contribute to ARC pathogenesis, although specific involvement is unclear. This study investigates regulating ferroptosis lens epithelial cells (LECs) and impact on progression. RNA sequencing anterior capsule samples from patients revealed a significant downregulation signaling, coupled with an upregulation ferroptosis-related genes. Notch1 expression decreased, while markers increased age-dependent manner. In vitro, alleviated by decreasing ferritin heavy chain 1 (FTH1) p53 levels enhancing nuclear factor erythroid 2-related 2 (Nrf2), glutathione peroxidase 4 (GPX4), solute carrier family 7 member 11 (SLC7A11). Conversely, inhibition exacerbated ferroptosis, as evidenced reduced Nrf2, GPX4, SLC7A11 expression. These findings suggest that promotes LECs impairing Nrf2/GPX4 antioxidant thereby contributing development. offers new insights into pathogenesis highlights pathway potential therapeutic target preventing or mitigating

Язык: Английский

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MiR-224-3p regulates ferroptosis and inflammation in lens epithelial cells by targeting ACSL4

Experimental Eye Research, Год журнала: 2025, Номер 254, С. 110306 - 110306

Опубликована: Фев. 20, 2025

Язык: Английский

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Advances in Sonodynamic Therapy: Focus on Ferroptosis

Journal of Medicinal Chemistry, Год журнала: 2025, Номер unknown

Опубликована: Март 10, 2025

Ferroptosis is a nonapoptotic form of cell death discovered in 2012. Noninvasive treatments regulating ferroptosis are important for wide range diseases. Among the noninvasive treatments, sonodynamic therapy (SDT) has become promising due to its strong tissue penetration and few side effects. In recent years, targeted drug delivery platforms constructed on basis SDT have provided an efficient mode regulation ferroptosis. Based latest research reports, this Perspective introduces basic mechanism influencing factors therapeutic effects, elucidates significance ferroptosis-targeted SDT, summarizes studies through different pathways. We also present innovative composite ultrasound-responsive platforms. Finally, brief summary outlook based current presented.

Язык: Английский

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Growth Arrest-specific 1 Inhibits Keap1/Nrf2 Signaling Transduction in the Activation of the Ferroptosis Program in Retinal Müller Cells

Frontiers in Bioscience-Landmark, Год журнала: 2025, Номер 30(3)

Опубликована: Март 18, 2025

Background: Diabetes retinopathy (DR) represents a microvascular disease in diabetes. Growth arrest-specific 1 (GAS1) is differentially expressed rat retinal Müller cells under high glucose (HG) conditions, and its promotion of ferroptosis contributes to cell death. However, the influence GAS1 DR elusive. Herein, we aimed investigate effect potential mechanism based on GAS1-mediated DR. Methods: After HG treatment, genes were analyzed by transcriptome sequencing followed Kyoto Encyclopedia Genes Genomes (KEGG) Gene Ontology (GO) analyses; finally, was selected. The effects knockdown/overexpression nuclear factor erythroid 2-related (Nrf2) silencing viability, apoptosis, lipid peroxidation, Fe2+, oxidative stress levels HG-induced/transfected measured Cell Counting Kit-8 (CCK-8) assay, flow cytometry, commercial reagent kits. Nrf2, especially GAS1, Kelch-like ECH-associated protein (Keap1) expressions cells, determined quantitative real-time polymerase chain reaction (qRT-PCR) or Western blot. Results: treatment decreased viability glutathione (GSH) increased reactive oxygen species (ROS), disulfide (GSSG), malondialdehyde (MDA), stress, Fe2+ (p < 0.01). also upregulated Keap1, total Nrf2 while downregulating 0.001). downregulation enhanced GSH levels, expression reducing ROS, GSSG, MDA, HG-treated 0.001), whereas overexpression had opposite effects. Additionally, reversed impact 0.05). Conclusion: inhibits Keap1/Nrf2 signaling transduction activating cells; thus, this study can aid setting stage for novel methods against

Язык: Английский

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