Age-related macular degeneration (AMD) is a leading cause of vision impairment worldwide, primarily driven by oxidative stress and inflammation. This review examines the role of antioxidants in mitigating oxidative damage, emphasizing both their therapeutic potential and limitations in AMD management. Key findings underscore the efficacy of specific antioxidants, including vitamins C and E, lutein, zeaxanthin, and Coenzyme Q10, in slowing AMD progression. Landmark studies such as AREDS and AREDS2 have shaped current antioxidant formulations, although challenges persist, including patient variability and long-term safety concerns. Emerging therapies, such as mitochondrial-targeted antioxidants and novel compounds like saffron and resveratrol, offer promising avenues for AMD treatment. Complementary lifestyle interventions, including antioxidant-rich diets and physical activity, further support holistic management approaches. This review highlights the critical role of antioxidants in AMD therapy, advocating for personalized strategies to optimize patient outcomes.

Amniotic membrane transplantation (AMT) has emerged as a versatile therapeutic modality with significant applications in wound healing, tissue regeneration, and ophthalmology. This review comprehensively evaluates AMT's efficacy in acute and chronic wound management, where it has been shown to alleviate pain, reduce infection risk, and facilitate epithelialization. In chronic wounds, AMT enhances healing through mechanisms such as re-epithelialization, angiogenesis, and immune modulation. Additionally, AMT exhibits promise in nerve regeneration, demonstrating potential in the repair of peripheral and central nervous system injuries by fostering neural recovery and minimizing scar formation. In ophthalmology, AMT is instrumental in corneal surface reconstruction, conjunctival repairs, and the management of dry eye syndrome and limbal stem cell deficiency. While the benefits of AMT are well-documented, this review also addresses significant challenges, including variability in success rates across different clinical conditions, ethical concerns regarding donor tissue usage, and regulatory hurdles impacting its broader clinical application. Furthermore, we integrate recent advances in the understanding of AMT's molecular mechanisms – such as its antioxidant effects via Nrf2/HO-1 pathway and immune modulation via P2X7 receptor pathways – and highlight innovative strategies including the incorporation of nanoceria nanoparticles, Vitamin D3 supplementation, and gene therapy approaches to enhance AMT outcomes. By exploring these dimensions, the review highlights not only the current state of AMT but also its potential future role in advancing regenerative medicine, including emerging applications in spinal cord repair, orthopaedics, and tissue engineering. This updated synthesis aims to inform clinicians and researchers about the multifaceted applications of AMT, promoting further investigation and optimization of this promising therapeutic approach. Graphical Abstract

Diabetic eye disease (DED) encompasses a range of ocular complications arising from diabetes mellitus, including diabetic retinopathy, diabetic macular edema, diabetic keratopathy, diabetic cataract, and glaucoma. These conditions are leading causes of visual impairments and blindness, especially among working-age adults. Despite advancements in our understanding of DED, its underlying pathophysiological mechanisms remain incompletely understood. Chronic hyperglycemia, oxidative stress, inflammation, and neurodegeneration play central roles in the development and progression of DED, with immune-mediated processes increasingly recognized as key contributors. This review provides a comprehensive examination of the complex interactions between immune cells, inflammatory mediators, and signaling pathways implicated in the pathogenesis of DED. By delving in current research, this review aims to identify potential therapeutic targets, suggesting directions of research for future studies to address the immunopathological aspects of DED.

Background/Objectives: Cataract surgery has evolved into a refractive procedure aimed at optimizing both vision quality and quantity. Modern patients, particularly “baby boomers”, expect superior outcomes, increasing demand for premium intraocular lenses (IOLs). However, ocular surface dysfunction (OSD), especially dry eye disease (DED), compromises postoperative satisfaction, with up to 35% of patients dissatisfied despite achieving 20/20 visual acuity. This study aimed to characterize postsurgical ocular surface system failure (OSSF) and explore strategies to improve perioperative management. Methods: An open observational study was conducted at the Ophthalmology Complex Operative Unit, University Campus Bio-Medico, Rome, Italy, enrolling 20 patients with stage N2–3 and C1–2 lens opacities. Patients with diabetes, prior surgeries, or ocular inflammatory diseases were excluded. Preoperative and postoperative assessments included OSDI, SANDE scores, Schirmer test, TBUT, and fluorescein staining. Follow-ups occurred at 1 week, 1 month, and 3 months postoperatively. Statistical analysis used two-way ANOVA (p < 0.05). Results: Despite achieving a BCVA of 20/20, 44% of patients reported OSSF symptoms. Postoperative evaluations revealed significant worsening in OSDI and SANDE scores (p < 0.001), Schirmer test (preoperative mean 19.92 ± 10.06; p < 0.001), and TBUT (preoperative mean 5.88 ± 2.64 s; p < 0.001). Meibomian gland dysfunction and conjunctival hyperemia also worsened. Conclusions: Postsurgical OSSF results from neurogenic inflammation, tear film instability, and meibomian gland dysfunction, exacerbated by surgical trauma. Preoperative and postoperative management, including artificial tears, lid hygiene, and preservative-free regimens, are essential to improve outcomes and patient satisfaction. Comprehensive strategies can mitigate symptoms and enhance the benefits of cataract surgery.

Retinal diseases, which can lead to significant vision loss, are complex conditions involving various cellular and molecular mechanisms. The interleukin-6 (IL-6) family, particularly Oncostatin M (OSM), has garnered attention for their roles in retinal inflammation, angiogenesis, and neuroprotection. This comprehensive review explores the dual nature of OSM and other IL-6 family members in retinal pathophysiology, highlighting their contribution to both degenerative and regenerative processes. The review also examines current research on OSM’s interaction with key signaling pathways and discusses the potential of OSM and the IL-6 family as potential therapeutic targets. Understanding these mechanisms could lead to innovative treatments that modulate OSM activity, offering new avenues for managing retinal diseases and contributing to the development of more effective interventions.

Cerebral ischemia remains a major global health challenge, contributing significantly to long-term disability and mortality, with limited therapeutic options currently available. This study explores the therapeutic potential of Mannosamine (ManN), an hexosamine previously shown to be a mitogen for endothelial cells (ECs), in the context of cerebral ischemic injury. Using a transient middle cerebral artery occlusion (tMCAO) mouse model, we assessed the effects of ManN administration on ischemic brain damage. Mice receiving ManN exhibited significantly smaller infarct volumes, as measured by magnetic resonance imaging (MRI), and reduced blood–brain barrier (BBB) permeability compared to controls. ManN treatment enhanced pericyte coverage, improved EC survival, and increased vascular density in the ischemic brain regions. Our analyses revealed attenuation of ischemia-induced structural abnormalities, including reduced vacuolation, cellular shrinkage, and nuclear condensation. To elucidate the underlying mechanisms, in vitro experiments with brain endothelial cells (bEND.3) demonstrated that ManN treatment promoted GSK3β phosphorylation and facilitated nuclear accumulation of β-catenin. This activation of the Wnt/β-catenin pathway led to upregulation of key target genes such as LEF1 , TCF7 , AXIN2 , and APCDD1 . Enhanced interaction of β-catenin with LEF1/TCF7 was associated with increased expression of tight junction proteins and transcytosis inhibitors, contributing to BBB stabilization and angiogenic support. Collectively, these findings highlight the ability of ManN to activate endothelial Wnt/β-catenin signaling, thereby preserving BBB integrity and promoting angiogenesis, suggesting its promise as a novel therapeutic strategy for cerebral ischemia.