Phytic acid-loaded polyvinyl alcohol hydrogels promotes wound healing of injured corneal epithelium through inhibiting ferroptosis

Redox Biology, Год журнала: 2024, Номер unknown, С. 103354 - 103354

Опубликована: Сен. 1, 2024

Язык: Английский

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A multifunctional nanoplatform with dual-targeted antibacterial and cascaded immunomodulatory strategy for the treatment of bacterial keratitis

Chemical Engineering Journal, Год журнала: 2024, Номер 498, С. 155323 - 155323

Опубликована: Авг. 30, 2024

Язык: Английский

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Unlocking the Potential of Antimicrobial Peptides: Cutting-Edge Advances and Therapeutic Potential in Combating Bacterial Keratitis

Bioconjugate Chemistry, Год журнала: 2025, Номер unknown

Опубликована: Фев. 19, 2025

Bacterial keratitis is a prevalent, and severe corneal illness resulting from bacterial pathogens. Failure to administer timely suitable therapy may lead opacity, ulceration, significant vision impairment, or potential blindness. Current clinical interventions for involve the administration of topical antimicrobial agents systemic antibiotics. However, misuse overuse antibiotics have led rapid emergence antibiotic-resistant bacteria. Additionally, restricted antibacterial spectrum possible adverse effects provided considerable obstacles traditional therapies. This highlights urgent need novel highly effective agents. Antimicrobial peptides (AMPs) are class naturally occurring synthetically designed small molecules that gained attention due their unique mechanisms low risk resistance development. AMPs exhibit promising in treating through direct mechanisms, such as inhibiting cell wall synthesis, disrupting membranes, interfering with nucleic acid metabolism, well indirect including modulation host immune response. review provides comprehensive overview advancements treatment keratitis. It emphasizes role various modification strategies artificial-intelligence-assisted design enhancing efficacy, stability, biocompatibility AMPs. Furthermore, this discusses latest progress combining delivery systems improved therapeutic outcomes. Finally, current challenges future perspectives treatment, providing valuable insights developing high safety

Язык: Английский

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Ferrostatin-1 inhibits tracheal basal cell ferroptosis to facilitate the rapid epithelization of 3D-printed tissue-engineered tracheas

Stem Cell Research & Therapy, Год журнала: 2025, Номер 16(1)

Опубликована: Март 24, 2025

Tracheal replacement is a promising approach for treating tracheal defects that are caused by conditions such as stenosis, trauma, or tumors. However, slow postoperative epithelial regeneration often leads to complications, infection and granulation tissue formation. Ferroptosis, which an iron-dependent form of regulated cell death, limits the proliferation basal cells (TBCs), essential epithelialization tissue-engineered tracheas (TETs). This study explored potential ferrostatin-1 (FER-1), ferroptosis inhibitor, increase TBC accelerate 3D-printed TETs. TBCs were isolated from rabbit bronchial mucosal tissues cultured in vitro. Ferroptosis was induced at passage 2, shown increased reactive oxygen species (ROS) levels, Fe2⁺ accumulation, decreased ATP contents, mitochondrial damage. treated with FER-1 (1 μM) 48 h inhibit ferroptosis. The effects on ROS morphology measured. For vivo experiments, FER-1-treated seeded onto polycaprolactone (PCL) scaffolds, implanted into rabbits injury. Epithelial formation evaluated 6 months after surgery. treatment significantly reduced marker levels vitro; is, ameliorated structures, levels. viability inhibition. In vivo, group received scaffolds exhibited accelerated TET compared control groups. These results suggest inhibiting improves function, leading more efficient repair. Ferrostatin-1 effectively inhibits cells, promoting their proliferation. faster tracheas, offering strategy improving reconstruction outcomes reducing complications Future studies needed further investigate molecular mechanisms underlying its clinical applications.

Язык: Английский

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Bifunctional chemokine-nanobody fusion protein enhances neutrophil recruitment to impede Acanthamoeba immune evasion

EBioMedicine, Год журнала: 2025, Номер 115, С. 105685 - 105685

Опубликована: Апрель 12, 2025

Язык: Английский

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Targeting prominin-2/BACH1/GLS pathway to inhibit oxidative stress-induced ferroptosis of bone mesenchymal stem cells

Stem Cell Research & Therapy, Год журнала: 2025, Номер 16(1)

Опубликована: Апрель 29, 2025

Suppressing bone mesenchymal stem cell (BMSC) ferroptosis is expected to optimize BMSCs-based therapy for intervertebral disc degeneration (IVDD). Our previous study revealed that Prominin-2 could protect against by decreasing cellular Fe2+ content and inhibiting transcription regulator protein BACH1 (BACH1) expression. In this we probed the molecular mechanisms underlying Prominin-2/BACH1 pathway in BMSC ferroptosis. Using an array of vitro vivo experiments found heat shock factor 1 (HSF1) activates PROM2 (encoding Prominin-2) elevated Furthermore, showed attenuates induced tert-butyl hydroperoxide (TBHP) through promoting ubiquitination degradation. Inhibition expression reversed TBHP-stimulated down glutaminase kidney isoform, mitochondrial (GLS), which plays a crucial role protecting BMSCs Targeting axis has also been shown improve survival post-transplantation mitigate IVDD progression results support new mechanistic insight into regulation Prominin-2/BACH1/GLS These finding lead potential therapeutic targets engrafted under oxidative stress circumstances.

Язык: Английский

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Chlamydia trachomatis infection induces ferroptosis and enhances chlamydial replication

Microbial Pathogenesis, Год журнала: 2025, Номер 205, С. 107656 - 107656

Опубликована: Май 1, 2025

Chlamydia trachomatis (C. trachomatis) has been shown to activate multiple programmed cell death pathways, which contribute significantly host immune responses. Nevertheless, the precise molecular mechanisms by C. induces remain poorly characterized. Ferroptosis, a recently identified form of iron-dependent, lipid peroxidation-driven regulated death, may represent previously unrecognized pathway in chlamydial pathogenesis. To investigate underlying trachomatis-induced we first performed transcriptomic analysis identify differentially expressed genes and enriched pathways infected HeLa cells. Concurrently, quantified intracellular iron levels, reactive oxygen species (ROS) accumulation, peroxidation, all are hallmarks ferroptosis. Transmission electron microscopy (TEM) further revealed distinct mitochondrial alterations trachomatis-infected cells, suggesting potential dysfunction cellular redox homeostasis. directly assess role ferroptosis infection, treated cells with ferroptosis-specific inhibitor Ferrostatin-1 (Fer-1) evaluated its effects on replication inflammatory Bioinformatic demonstrated significant enrichment homeostasis ferroptosis-related signaling exhibiting particularly strong activation. Experimentally, infection disrupted expression key transporters (e.g., TFR FPN1), causing dysregulated uptake storage. downregulated critical inhibitors SLC7A11 GPX4, leading elevated peroxidation. Ultrastructural via TEM pronounced abnormalities including marked swelling cristae disintegration-a hallmark ferroptotic damage. Notably, pharmacological inhibition using Fer-1 not only attenuated infection-induced but also suppressed bacterial replication, as host-pathogen interaction nexus. This study provides evidence that targeting novel therapeutic strategy for controlling infections.

Язык: Английский

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Exploring the potential of nanoparticles-based polydopamine for effective treatment of refractory keratitis: Mild photothermal loop therapy

International Journal of Biological Macromolecules, Год журнала: 2024, Номер 279, С. 135479 - 135479

Опубликована: Сен. 8, 2024

Язык: Английский

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