Age-related macular degeneration (AMD) causes vision loss in the elderly population. Dry AMD leads to the formation of Drusen, while wet AMD is characterized by cell proliferation and choroidal angiogenesis. The retinal pigment epithelium (RPE) plays a key role in AMD pathogenesis. In particular, helioreceptor renewal depends on outer segment phagocytosis of RPE cells, while RPE autophagy can protect cells from oxidative stress damage. However, when the oxidative stress burden is too high and homeostasis is disturbed, the phagocytosis and autophagy functions of RPE become damaged, leading to AMD development and progression. Hence, characterizing the roles of RPE cell phagocytosis and autophagy in the pathogenesis of AMD can inform the development of potential therapeutic targets to prevent irreversible RPE and photoreceptor cell death, thus protecting against AMD.

Scar formation resulting from overly active wound healing is a critical factor in the success rate of glaucoma filtration surgery (GFS). IL-6 and TGF-β have been implicated in the pathogenesis of fibrogenesis. In addition, the signal transducer and activator of transcription 3 (STAT3) can be activated by numerous cytokines and growth factors, including IL-6 and TGF-β1. Thus, STAT3 activation may integrate common profibrotic pathways to promote fibrosis. In this study, an increase in p-STAT3 was observed in activated HTFs. Inhibiting STAT3 in cultured HTFs by pharmacological inactivation reversed the fibrotic responses, such as fibroblast migration, the differentiation of resting fibroblasts into myofibroblasts and the deposition of ECM, mediated by IL-6 and TGF-β1. Moreover, the expression of suppressor of cytokine signaling 3 (SOCS3) was decreased in HTFs cultured with IL-6 and TGF-β1, and SOCS3 overexpression rescued ECM deposition, α-SMA expression and migration in IL-6- and TGF-β1-stimulated HTFs by inactivating STAT3. Finally, S3I-201 treatment inhibited profibrotic gene expression and subconjunctival fibrosis in a rat model of GFS. In conclusion, our data suggests that STAT3 plays a central role in fibrosis induced by different profibrotic pathways and that STAT3 is a potential target for antifibrotic therapies following GFS.

Glaucoma represents a predominant cause of irreversible blindness globally, characterized by the association of elevated intraocular pressure (IOP) and ret

AIM: To employ proteome-wide Mendelian randomization (MR) to explore novel protein and drug targets for retinal neurodegenerative diseases (RND) in individuals of European ancestry. METHODS: This study used summary data-based MR to analyze the correlation between plasma protein levels and three RND, with protein data derived from two independent large-scale proteomics datasets. Potential drug targets were identified using Bayesian colocalization, followed by MR analysis, sensitivity testing, and external validation. Drug prediction and molecular docking were conducted to evaluate the druggability of the target proteins. RESULTS: The study identified six promising protein targets, each successfully replicated at least twice. The results included three proteins related to diabetic retinopathy (ICAM1, GCKR, WARS), two proteins related to age-related macular degeneration (WARS, BRD2), and two proteins related to glaucoma (SVEP1, NPTXR). Additionally, drug prediction and molecular docking indicated that five drugs (fenofibrate, trofinetide, ticagrelor, lifitegrast, acetaminophen) effectively bound to the target proteins. CONCLUSION: This study identified six potential protein targets for RND and five existing drugs with therapeutic potential. By integrating plasma proteomics with genetic data, it provides a cost-effective framework for drug discovery.

Glaucoma frequently coexists with cataract, but glaucomatous functional loss, ocular‐surface disease, anatomical abnormalities, and treatment‐related refractive variability may reduce tolerance of premium intraocular lenses. This narrative review critically appraises evidence relevant to lens selection in glaucoma. Central visual‐field status, contrast sensitivity, fixation, disease stability, anterior‐segment anatomy, intraocular pressure control, topical treatment, previous or anticipated glaucoma surgery, and lifetime progression risk should inform decision‐making. Enhanced monofocal lenses may improve intermediate vision while preserving distance vision and functional reserve in selected patients with ocular hypertension, preperimetric glaucoma, or early, stable open‐angle glaucoma. Selected extended depth‐of‐focus lenses may be considered when central visual function is preserved, whereas toric lenses require regular, repeatable astigmatism and stable capsular‐zonular support. Current evidence does not support routine multifocal lens implantation in established glaucoma. Selection should remain individualised, evidence‐calibrated and supported by explicit counselling about uncertainty, dysphotopsias, future progression and possible refractive change after glaucoma surgery.