Dry eye disease (DED) is increasingly recognized as a condition driven by immune dysregulation at the ocular surface (OS). Chronic inflammation, mediated by aberrant activation of both innate and adaptive immune pathways, underlies disease progression and symptom persistence. Neuroimmune interactions further amplify OS inflammation, contributing to epithelial damage and impaired homeostatic regulation. This review summarizes current literature on the immunopathogenesis of DED, highlighting the complex interplay of molecular mechanisms of innate and adaptive immune activation, neuroimmune-mediated inflammation, and emerging molecular and cellular biomarkers. In addition, we examine existing and emerging therapeutic strategies that target these immune-molecular pathways, including precision immunomodulatory approaches, to inform future management of DED. By integrating mechanistic insights with clinical findings, this review aims to provide a comprehensive overview of the molecular mechanisms underlying the dysregulated immune response associated with DED.

Pseudoexfoliation syndrome (PXS) is an age-related fibrillopathy where fibrillar exfoliation material accumulates and deposits in ocular and extra-ocular tissue. Within the eye, this substance accumulates on the ocular surface and in the anterior segment of the eye, impacting ocular structures such as the conjunctiva, Tenon’s capsule, sclera, cornea, iris, ciliary body, trabecular meshwork, and lens. This review aims to collate the current literature on how each anatomical part of the eye is affected by PXS, with a strong focus on molecular changes. We also summarise the current understanding of the key genetic factors influencing the development of PXS.

Dry eye disease is increasingly recognised as a condition driven by immune dysregulation at the ocular surface. Chronic inflammation, mediated by aberrant activation of both innate and adaptive immune pathways, underlies disease progression and symptom persistence. Neuroimmune interactions further amplify ocular surface inflammation, contributing to epithelial damage and impaired homeostatic regulation. This review synthesizes current literature on the immunopathogenesis of dry eye disease (DED), highlighting the complex interplay of molecular mechanisms of innate and adaptive immune activation, neuroimmune-mediated inflammation, and emerging molecular and cellular biomarkers. In addition, we examine existing and emerging therapeutic strategies that target these immune-molecular pathways, including precision immunomodulatory approaches, to inform future management of DED. By integrating mechanistic insights with clinical findings, this review aims to provide a comprehensive overview of the molecular mechanisms underlying the dysregulated immune response associated with DED.

Genome editing has emerged as a transformative approach for understanding and treating retinal degenerative diseases. Combining this technology with pluripotent stem cells provides an ideal platform for modeling human development and disease, and investigating emerging therapeutic strategies ultimately aimed towards in vivo correction. This approach enables both functional studies to understand retinal degeneration and the early development of targeted therapies for inherited disease. This review offers a comprehensive overview of genome-editing techniques and the ability to create new clinically relevant models to understand human disease in retinal research, focusing on the use of the CRISPR-Cas9 system in induced pluripotent stem cells (iPSCs) and embryonic stem cells (ESCs), as well as highlighting recent advancements in base and prime editing. Gene editing in various retinal diseases is discussed in context of studies focusing on disease modeling or developing therapeutic strategies. Continued refinement of these techniques will be essential for advancing translational applications in retinal disease treatment.

Diabetic retinopathy (DR) is a major cause of preventable blindness in working-age adults, yet the molecular mechanisms behind its vision-threatening complications remain not fully understood. Transcriptomics enables the study of these processes through active gene expression, providing a pathway to the discovery of new biomarkers and therapeutic targets. Vitreous humour is commonly affected in numerous retinal pathologies, including DR, and is accessible through pars plana vitrectomy, making it a good candidate for transcriptomics research. Following PubMed and Embase search, 18 articles on vitreous transcriptomics were included. They were subclassified into themes of non-coding RNA, RNA methylation, angiogenesis, inflammation and fibrosis. We concluded that vitreous transcriptomics has the potential to influence future DR diagnostics and therapeutics. However, current evidence is limited by underpowered studies and lack of standardised protocols.