Purpose: Ischemic stroke is a refractory disease wherein the reperfusion injury caused by sudden restoration of blood supply is the main cause of increased mortality and disability. However, current therapeutic strategies for the inflammatory response induced by cerebral ischemia-reperfusion (I/R) injury are unsatisfactory. This study aimed to develop a functional nanoparticle (MM/ANPs) comprising apelin-13 (APNs) encapsulated in macrophage membranes (MM) modified with distearoyl phosphatidylethanolamine-polyethylene glycol-RVG29 (DSPE-PEG-RVG29) to achieve targeted therapy against ischemic stroke. Methods: MM were extracted from RAW264.7. PLGA was dissolved in dichloromethane, while Apelin-13 was dissolved in water, and CY5.5 was dissolved in dichloromethane. The precipitate was washed twice with ultrapure water and then resuspended in 10 mL to obtain an aqueous solution of PLGA nanoparticles. Subsequently, the cell membrane was evenly dispersed homogeneously and mixed with PLGA-COOH at a mass ratio of 1:1 for the hybrid ultrasound. DSPE-PEG-RVG29 was added and incubated for 1 h to obtain MM/ANPs. Results: In this study, we developed a functional nanoparticle delivery system (MM/ANPs) that utilizes macrophage membranes coated with DSPE-PEG-RVG29 peptide to efficiently deliver Apelin-13 to inflammatory areas using ischemic stroke therapy. MM/ANPs effectively cross the blood-brain barrier and selectively accumulate in ischemic and inflamed areas. In a mouse I/R injury model, these nanoparticles significantly improved neurological scores and reduced infarct volume. Apelin-13 is gradually released from the MM/ANPs, inhibiting NLRP3 inflammasome assembly by enhancing sirtuin 3 (SIRT3) activity, which suppresses the inflammatory response and pyroptosis. The positive regulation of SIRT3 further inhibits the NLRP3-mediated inflammation, showing the clinical potential of these nanoparticles for ischemic stroke treatment. The biocompatibility and safety of MM/ANPs were confirmed through in vitro cytotoxicity tests, blood-brain barrier permeability tests, biosafety evaluations, and blood compatibility studies. Conclusion: MM/ANPs offer a highly promising approach to achieve ischemic stroke-targeted therapy inhibiting NLRP3 inflammasome-mediated pyroptosis.

Aim: Targeted retinal photocoagulation (TRP) is an emerging laser technology for retinal targeted therapy. TRP can specifically act on unperfused retinal capillaries and retinal intermediate ischemic areas, reduce damage to tissue perfusion areas and panretinal photocoagulation (PRP) complications or adverse events. In this regard, this review discusses the treatment options, efficacy, and latest progress of TRP for diabetic retinopathy (DR) based on randomized controlled trial (RCT), meta-analysis, case review, and other existing studies.Methods: In-depth research was conducted on articles about the proposal and development of TRP, its simple application in DR, and combined therapy. In order to review the new progress, application methods, effects, and prospects of TRP in the treatment of DR, the articles related to TRP in the databases of PubMed and Web Of Science since this century were comprehensively analyzed.Results: TRP is effective in treating DR and may become a substitute for PRP in the future. In addition, the treatment regimen of TRP combined with intravitreal injection of anti-vascular endothelial growth factor (anti-VEGF) drugs can also be used as a new therapeutic approach to expand the treatment regimen for the treatment of DR, and this combination therapy also has effects on other retinal vascular diseases.Conclusions: With the advancement of technology, TRP has been continuously applied in clinical practice, and its potential benefits have opened up broad prospects for the treatment of DR. The combination therapy of TRP and anti-VEGF is expected to become a new option for patients with DR an retinal diseases.

The repair mechanism for corneal epithelial cell injuries encompasses migration, proliferation, and differentiation of corneal epithelial cells, and extracellular matrix remodeling of the stromal structural integrity. Furthermore, it involves the consequential impact of corneal limbal stem cells (LSCs). In recent years, as our comprehension of the mediating mechanisms underlying corneal epithelial injury repair has advanced, it has become increasingly apparent that growth factors play a pivotal role in this intricate process. These growth factors actively contribute to the restoration of corneal epithelial injuries by orchestrating responses and facilitating specific interactions at targeted sites. This article systematically summarizes the role of growth factors in corneal epithelial cell injury repair by searching relevant literature in recent years, and explores the limitations of current literature search, providing a certain scientific basis for subsequent basic research and clinical applications.

The gut microbiota modulates aging through metabolic and immune interactions. To characterize microbial changes during aging, we profiled gut microbiota across four stages in male C57BL/6J mice: young-adult, middle-aged, senescent, and frailty. Using 16S rRNA sequencing and targeted metabolomics, we observed a biphasic diversity pattern, with reduced richness in senescence followed by a rebound in frailty. Frailty-stage microbiota showed increased connectivity and enrichment of Lachnospiraceae, alongside short-chain fatty acid (SCFA) depletion, particularly butanoic acid. Functional predictions revealed elevated immune activity and reduced carbohydrate metabolism, linked to specific microbial taxa. These findings highlight a structured remodeling of the gut microbiota during aging, with frailty representing a distinct dysbiotic state associated with metabolic dysfunction. Modulating gut microbial composition may represent a potential strategy to attenuate frailty and promote healthy aging.

Background: Ocular diseases pose a significant threat to visual health, with ferritin ferroptosis playing a critical role in the pathogenesis of many such conditions. Ferritin accumulation, coupled with ferritin autophagy-mediated release of labile Fe²⁺, triggers iron-dependent lipid peroxidation and ferroptosis. These include disruptions in iron metabolism, oxidative stress imbalances, altered intracellular signaling, and changes to the local microenvironment. Such aberrant ferritin deposits not only compromise the structure and function of ocular cells but also accelerate disease progression. Ferroptosis, a newly recognized form of cell death characterized by iron-dependent lipid peroxidation, differs from traditional cell death mechanisms, including apoptosis.Materials and methods: This review systematically evaluated the role of ferroptosis in ocular diseases using a predefined search strategy. In brief, PubMed was searched for studies published between 2012 and 2025 using keywords combining ferroptosis, ocular diseases, retinal, corneal etc. After excluding non-ocular studies and duplicates, 188 articles were included following a full-text review.Conclusion: This review examines the molecular mechanisms underlying ferroptosis and its implications for major ocular diseases. It explores how ferroptosis contributes to disease pathology in retinal diseases, offering novel insights for future therapeutic strategies. The potential for targeting ferroptosis pathways with iron modulators holds promise for advancing clinical treatments in ophthalmology.