Chao Chen

Oxidative stress-induced photoreceptor cell death is closely associated with the etiology of age-related macular degeneration (AMD), and sodium iodate (SI) has been widely used as an oxidant stimulus in AMD models to induce retinal pigment epithelium (RPE) and photoreceptor cell death. However, the mechanism underlying SI-induced photoreceptor cell death remains controversial and unclear. In this study, we elucidate that ferroptosis is a critical form of cell death induced by SI in photoreceptor-derived 661W cells. SI disrupts system Xc⁻, leading to glutathione (GSH) depletion and triggering lipid peroxidation, thereby promoting ferroptosis in photoreceptor-derived 661W cells. Additionally, SI enhances intracellular Fe²⁺ levels, which further facilitates reactive oxygen species (ROS) accumulation, making the 661W cells more susceptible to ferroptosis. Exogenous GSH, as well as specific inhibitors of ferroptosis such as Fer-1 and antioxidants like NAC, significantly attenuate SI-induced ferroptosis in photoreceptor-derived 661W cells. These findings provide new insights into the mechanisms of ferroptosis as a key pathway in SI-induced photoreceptor-derived 661W cell death.

Background Type 2 diabetes (T2D) and non-alcoholic fatty liver disease (NAFLD) are prevalent metabolic disorders with overlapping pathophysiological mechanisms. A comprehensive understanding of the shared molecular pathways involved in these conditions can advance the development of effective therapeutic interventions. Methods We used two datasets sourced from the Gene Expression Omnibus (GEO) database to identify common differentially expressed genes (DEGs) between T2D and NAFLD. Subsequently, we conducted Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses to identify the enriched biological processes and signaling pathways. In addition, we performed a protein-protein interaction (PPI) network analysis to identify hub genes with pivotal roles. To validate our findings, we established a type 2 diabetic mouse model with NAFLD. Results Our analysis identified 53 DEGs shared between T2D and NAFLD. Enrichment analysis revealed their involvement in signal transduction, transcriptional regulation, and cell proliferation as well as in the ferroptosis signaling pathways. PPI network analysis identified ten hub genes, namely CD44, CASP3, FYN, KLF4, HNRNPM, HNRNPU, FUBP1, RUNX1, NOTCH3, and ANXA2. We validated the differential expression of FYN, HNRNPU, and FUBP1 in liver tissues of a type 2 diabetic mouse model with NAFLD. Conclusions Our study offers valuable insights into the shared molecular mechanisms underlying T2D and NAFLD. The identified hub genes and pathways present promising prospects as therapeutic targets to address these prevalent metabolic disorders.

Ectodysplasin A (EDA), a ligand of the TNF family, plays an important role in maintaining the homeostasis of the ocular surface. EDA is necessary for the development of the meibomian gland, the lacrimal gland, as well as the proliferation and barrier function of the corneal epithelium. The mutation of EDA can induce the destruction of the ocular surface resulting in keratopathy, abnormality of the meibomian gland and maturation of the lacrimal gland. Experimental animal studies showed that a prenatal ultrasound-guided intra-amniotic injection or postnatal intravenous administration of soluble recombinant EDA protein can efficiently prevent the development of ocular surface abnormalities in EDA mutant animals. Furthermore, local application of EDA could restore the damaged ocular surface to some extent. Hence, a recombinant EDA-based therapy may serve as a novel paradigm to treat ocular surface disorders, such as meibomian gland dysfunction and corneal epithelium abnormalities.

Hyperbaric oxygenation (HBO) on postoperative rehabilitation of brain tumors and effects on tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) levels were explored. A retrospective analysis of 132 patients with brain tumors treated in the People's Hospital of Rizhao from October 2014 to October 2017 was performed. There were 62 patients in the observation group and 70 patients in the control group. Patients in the control group were treated with conventional drugs, and patients in the observation group were treated with HBO on the basis of conventional drug therapy. Levels of serum TNF-α and IL-6 were measured by ELISA before and after treatment. Cerebral arterial flow velocity and spasticity were measured by cranial color Doppler ultrasonography. Neurological function deficit (NFD) and activities of daily living (ADL) were used to evaluate the clinical recovery of the patients. Clinical efficacy was compared and analyzed. There were no significant differences between the two groups before treatment (P>0.05). After treatment, serum TNF-α and IL-6 levels were significantly lower than pretreatment levels (P<0.05), and serum TNF-α and IL-6 levels in the observation group were lower than those in the control group (P<0.05). Cerebral arterial flow velocity in observation group after treatment was significantly lower than that in the control group. The number of patients with cerebral arterial spasm after treatment in the observation group was significantly smaller than that in the control group. NFD scores in the observation group were lower than those in the control group after treatment. After treatment, ADL scores in the observation group were significantly higher than those in the control group (P<0.05). The comprehensive treatment effect of HBO is significant. It can inhibit the expression of inflammatory factors in serum and reduce cerebral arterial flow velocity and effectively reduce the number of patients with cerebral arterial spasm. It can reduce NFD and improve the quality of life of patients. Therefore, it is worthy of clinical popularization.