miR-214-3p attenuates ferroptosis-induced cellular damage in a mouse model of diabetic retinopathy through the p53/SLC7A11/GPX4 axis

Experimental Eye Research, Год журнала: 2025, Номер 253, С. 110299 - 110299

Опубликована: Фев. 18, 2025

Язык: Английский

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Ferroptosis: mechanisms and advances in ocular diseases

Molecular and Cellular Biochemistry, Год журнала: 2023, Номер 478(9), С. 2081 - 2095

Опубликована: Янв. 8, 2023

Язык: Английский

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Abietic acid inhibits acetaminophen-induced liver injury by alleviating inflammation and ferroptosis through regulating Nrf2/HO-1 axis

International Immunopharmacology, Год журнала: 2023, Номер 118, С. 110029 - 110029

Опубликована: Март 22, 2023

Язык: Английский

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Immunological Landscape of Retinal Ischemia-Reperfusion Injury: Insights into Resident and Peripheral Immune Cell Responses

Aging and Disease, Год журнала: 2024, Номер unknown

Опубликована: Янв. 1, 2024

Retinal ischemia-reperfusion injury (RIRI) is a complex condition characterized by immune cell-mediated inflammation and consequent neuronal damage. This review delves into the response mechanisms in RIRI, particularly emphasizing roles played resident peripheral cells. It highlights pivotal role of microglia, primary cells, exacerbating neuroinflammation damage through their activation subsequent release pro-inflammatory mediators. Additionally, explores contributions other glial cell types, such as astrocytes Müller modulating within retinal environment. The dual complement system RIRI also examined, revealing its functions both safeguarding impairing health. Inflammasomes, triggered various danger signals, are discussed crucial contributors to inflammatory pathways with an emphasis on involvement different NOD-like receptor family proteins. further analyzes infiltration impact cells like neutrophils, macrophages, T which migrate retina following ischemic injury. Critical this discussion interplay between implications for pathophysiology. Finally, outlines future research directions, focusing basic potential clinical translation enhance understanding treatment RIRI.

Язык: Английский

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Signalling pathways and cell death mechanisms in glaucoma: Insights into the molecular pathophysiology

Molecular Aspects of Medicine, Год журнала: 2023, Номер 94, С. 101216 - 101216

Опубликована: Окт. 17, 2023

Glaucoma is a complex multifactorial eye disease manifesting in retinal ganglion cell (RGC) death and optic nerve degeneration, ultimately causing irreversible vision loss. Research recent years has significantly enhanced our understanding of RGC degenerative mechanisms glaucoma. It evident that high intraocular pressure (IOP) not the only contributing factor to glaucoma pathogenesis. The equilibrium pro-survival pro-death signalling pathways retina strongly influences function survival RGCs axons Molecular evidence from human tissue analysis range experimental models have contributed unravelling these mechanisms. Accumulating reveals wide molecular can operate -either alone or via intricate networks - induce neurodegeneration. roles several molecules, including neurotrophins, interplay intracellular kinases phosphates, caveolae adapter proteins, serine proteases their inhibitors, nuclear receptors, amyloid beta tau, how dysfunction affects neurons are discussed this review. We further underscore anatomical alterations various animal exhibiting degeneration susceptibility glaucoma-related neuronal damage helped characterise In addition, we also present different regulated play critical role

Язык: Английский

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Chitosan-Rapamycin Carbon Dots Alleviate Glaucomatous Retinal Injury by Inducing Autophagy to Promote M2 Microglial Polarization

International Journal of Nanomedicine, Год журнала: 2024, Номер Volume 19, С. 2265 - 2284

Опубликована: Март 1, 2024

Introduction: Glaucoma is a prevalent cause of irreversible vision impairment, characterized by progressive retinal ganglion cells (RGCs) loss, with no currently available effective treatment.Rapamycin (RAPA), an autophagy inducer, has been reported to treat glaucoma in rodent models promoting RGC survival, but its limited water solubility, systemic toxicity, and pre-treatment requirements hinder potential clinical applications.Methods: Chitosan (CS)-RAPA carbon dot (CRCD) was synthesized via hydrothermal carbonization CS RAPA transmission electron microscopy, Fourier transform infrared spectra, proton nuclear magnetic resonance.In vitro assays on human umbilical cord vein endothelial rat cell line examined biocompatibility anti-oxidative capabilities, while lipopolysaccharide-stimulated murine microglia (BV2) measured effects microglial polarization.In vivo, using mouse ischemia/reperfusion (I/R) model acute intraocular pressure elevation, the CRCD visual function, apoptosis, oxidative stress, M2 polarization were examined.Results: exhibited good solubility form free radical scavenging.In vitro, bio-compatible lowered which also found vivo I/R model.Additionally, both BV2 model, able promote activating autophagy, which, turn, down-regulated pro-inflammatory cytokines, such as IL-1β TNF-α, well up-regulated anti-inflammatory IL-4 TGF-β.All these ultimately aided preserving RGCs, subsequently, improved function.Discussion: could serve novel treatment strategy for glaucoma, incorporating into CDs, turn not only mitigating toxic side enhancing therapeutic efficacy.

Язык: Английский

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N,N-Dimethyl-3β-hydroxycholenamide attenuates neuronal death and retinal inflammation in retinal ischemia/reperfusion injury by inhibiting Ninjurin 1

Journal of Neuroinflammation, Год журнала: 2023, Номер 20(1)

Опубликована: Апрель 7, 2023

Retinal ischemia-reperfusion (RIR) injury refers to an obstruction in the retinal blood supply followed by reperfusion. Although molecular mechanism underlying ischemic pathological cascade is not fully understood, neuroinflammation plays a crucial part mortality of ganglion cells.Single-cell RNA sequencing (scRNA-seq), docking, and transfection assay were used explore effectiveness pathogenesis N,N-dimethyl-3β-hydroxycholenamide (DMHCA)-treated mice with RIR DMHCA-treated microglia after oxygen glucose deprivation/reoxygenation (OGD/R).DMHCA could suppress inflammatory gene expression attenuate neuronal lesions, restoring structure vivo. Using scRNA-seq on retina mice, we provided novel insights into immunity demonstrated nerve injury-induced protein 1 (Ninjurin1/Ninj 1) as promising treatment target for RIR. Moreover, Ninj1, which was increased OGD/R-treated microglia, downregulated group. DMHCA suppressed activation nuclear factor kappa B (NF-κB) pathways induced OGD/R, undermined NF-κB pathway agonist betulinic acid. Overexpressed Ninj1 reversed anti-inflammatory anti-apoptotic function DMHCA. Molecular docking indicated that had low binding energy - 6.6 kcal/mol, suggesting highly stable binding.Ninj1 may play pivotal role microglia-mediated inflammation, while be potential strategy against injury.

Язык: Английский

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Modulating amacrine cell–derived dopamine signaling promotes optic nerve regeneration and preserves visual function

Science Advances, Год журнала: 2024, Номер 10(31)

Опубликована: Авг. 2, 2024

As part of the central nervous system, optic nerve, composed axons from retinal ganglion cells (RGCs), generally fails to regenerate on its own when injured in adult mammals. An innovative approach promoting nerve regeneration involves manipulating interactions between amacrine (ACs) and RGCs. Here, we identified a unique AC subtype, dopaminergic ACs (DACs), that responded early after crush by down-regulating neuronal activity reducing dopamine (DA) release. Activating DACs or augmenting DA release with levodopa demonstrated neuroprotective effects modestly enhanced axon regeneration. Within this context, pinpointed receptor D1 (DRD1) as critical mediator DAC-derived showed RGC-specific Drd1 overexpression effectively overcame subtype-specific barriers This strategy markedly boosted RGC survival preserved vision glaucoma model. study unveils crucial role signaling regeneration, holding promise for therapeutic insights into neural repair.

Язык: Английский

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Based on bioinformatics, SESN2 negatively regulates ferroptosis induced by ischemia reperfusion via the System Xc−/GPX4 pathway

Frontiers in Genetics, Год журнала: 2025, Номер 15

Опубликована: Янв. 29, 2025

Introduction Cerebral ischemia–reperfusion (IR) causes severe secondary brain injury. Previous studies have demonstrated that ferroptosis is involved in IR-induced However, whether IR induces microvascular endothelial cells (BMVECs) not fully understood. Materials and methods Oxygen–glucose deprivation/reoxygenation (OGDR) was performed bEND.3 to mimic injury vitro , a focal cerebral model created C57BL/6 mice. Transcriptomic sequencing of the first, followed by bioinformatics analysis. Differentially expressed gene (DEG) enrichment analysis highlighted ferroptosis-related pathways. Results Using Venn analysis, nine DEGs were identified, namely, Slc3a2 Slc7a11 Ccn2 Tfrc Atf3 Chac1 Gch1 Lcn2 Sesn2 . Protein–protein interaction (PPI) combined with molecular complex detection (MCODE) identified six hub genes, Ddit3 Trib3 Ppp1r15a Gadd45a Spearman’s correlation revealed significant between genes DEGs. After reperfusion, levels indicators elevated, expression proteins Xc− GPX4 decreased. SESN2 key antioxidant regulator. silencing reduced System GPX4, whereas overexpression promoted GPX4. Discussion These results suggest negative regulator ferroptosis. Enhancing can alleviate through activation Xc−/GPX4 pathway. By integrating mechanistic exploration, this study plays crucial role BMVECs injury, acting as via

Язык: Английский

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Ganoderma lucidum polysaccharide attenuates retinal ischemia-reperfusion injury by regulating microglial M1/M2 polarization, suppressing neuroinflammation and inhibiting JAK2/STAT3 pathway

Biochemistry and Biophysics Reports, Год журнала: 2025, Номер 41, С. 101926 - 101926

Опубликована: Янв. 29, 2025

Язык: Английский

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