Chemotherapy plays a major role in the treatment of cancer, but it still has great limitations in anti-tumor effect. Carboplatin (CAR) is the first-line drug in the treatment of non-small cell lung cancer, but the therapeutic effect is demonstrated weak. Therefore, we modified CAR with hexadecyl chain and polyethylene glycol, so as to realize its liposolubility and PEGylation. The synthesized amphiphilic CAR prodrugs could self-assemble into polymer micelles in water with an average particle size about 11.8 nm and low critical micelles concentration (0.0538 mg·mL^–1). In vivo pharmacodynamics and cytotoxicity experiment evidenced that the polymer micelles were equipped with preferable anti-tumor effect, finally attained the aim of elevating anti-tumor effect and prolonging retention time in vivo. The self-assembled micelles skillfully solve the shortcomings of weak efficacy of CAR, which provides a powerful platform for the application of chemical drug in oncology.

This study aims to systematically elucidate the burden of blindness and vision loss (BVL) attributable to smoking from 1990 to 2021 and to forecast the trends in BVL burden over the next decade. We extracted data on years lived with disability (YLDs) and age-standardized YLDs rate (ASYR) related to blindness and vision loss (BVL) caused by smoking, including cataracts and age-related macular degeneration (AMD), from the Global Burden of Disease (GBD) database for the years 1990 to 2021. These data were disaggregated by age, gender, sociodemographic index (SDI), region, and country. Temporal trends in the burden of smoking-induced BVL were evaluated by calculating the average annual percentage changes (AAPCs). BVL attributable to smoking presents a significant disease burden, with global BVL-related YLDs attributable to smoking increasing from 1990 to 2021, while ASYR showed a declining trend. In 2021, the global BVL-related YLDs and ASYR attributable to smoking were estimated at 284.03 thousand and 3.27 per 100,000 population. The ASYR for cataract and AMD are 2.60 and 0.68 per 100,000, respectively. The burden was notably higher in males than females, highlighting significant gender disparities. Regionally, the highest burdens were observed in South Asia, Southeast Asia, and North Africa. It is expected that the number of global BVL-related YLDs will increase further by 2030. Smoking has imposed a substantial disease burden on BVL over the past three decades. The burden is predominantly concentrated among males, particularly older individuals and those in low to middle-SDI regions. Moreover, the burden of smoking-induced BVL is expected to continue improving over the next decade.

Glaucoma, a leading cause of irreversible blindness, is characterized by progressive retinal ganglion cell (RGC) degeneration with limited treatment options. The natural flavonoid farrerol exhibits neuroprotective potential through antioxidative and anti-inflammatory effects, but its therapeutic application is limited by poor bioavailability and photodegradation. This study investigates farrerol's neuroprotective mechanisms and develops an optimized nanoformulation for enhanced efficacy. In vitro oxygen-glucose deprivation/reperfusion (OGD/R) and in vivo ischemia-reperfusion (IR) models demonstrate that farrerol significantly improves RGC survival and visual function. Mechanistic studies reveal that farrerol activates the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway, reduces reactive oxygen species (ROS) accumulation, and modulates key ferroptosis markers (glutathione peroxidase 4 (GPX4) and acyl-CoA synthetase long-chain family member 4 (ACSL4)), thereby inhibiting RGC apoptosis. To overcome delivery limitations, farrerol-loaded bilirubin nanoparticles (FB-NPs) are developed, showing enhanced stability and neuroprotective effects in glaucomatous injury models. These findings identify the Nrf2/ferroptosis/apoptosis axis as a novel therapeutic target and present an effective nanodelivery strategy for glaucoma treatment.

Glaucoma is the primary factor underlying irreversible blindness. Recent studies suggest that the risk of glaucoma significantly increases in patients with systemic lupus erythematosus (SLE); however, the mechanism underlying this association remains unclear. Therefore, this study aimed to identify novel common biomarkers and potential therapeutic drugs for SLE and glaucoma. GSE27276, GSE50772, and GSE148371 datasets were sourced from the gene expression omnibus (GEO) database. An integrated analysis of the datasets for both diseases identified biomarkers and thoroughly examined their biological roles and molecular mechanisms using differential expression analysis (DEA), weighted gene co‐expression network analysis (WGCNA), gene enrichment analysis, machine learning, microRNA (miRNA) and transcription factor analyses, immune infiltration analyses, and single‐cell transcriptome analysis. Concurrently, molecular docking was used to forecast potential drugs targeting these biomarkers. Finally, reverse transcription quantitative real‐time polymerase chain reaction (RT‐qPCR) was performed in human trabecular meshwork stem cells to validate the five identified biomarkers. The 10 key genes identified through DEA and WGCNA were predominantly involved in immune, inflammatory, and autophagy pathways. Additionally, machine learning identified five biomarkers, and we established associated transcription factors and miRNA regulatory networks. Immune infiltration analysis indicated an elevated presence of immune cells, including macrophages, T cells, and B cells, in both conditions. Furthermore, the DSigDB database yielded 10 potential therapeutic agents, three of which showed strong binding potential to the biomarkers via molecular docking. The RT‐qPCR results confirmed the trend in gene expression. This study uncovered a new link between SLE and primary open‐angle glaucoma, identifying biomarkers and mechanisms of immunopathogenesis for future research and treatment strategies.

The online version contains supplementary material available at 10.1038/s41598-026-41588-y.