Research Area: " Basic Ophthalmology Research; Ocular diseases involving angiogenesis pathophysiology "

My lab research focuses on translational ophthalmology, with a particular emphasis on angiogenesis-driven ocular diseases. We investigate the molecular and cellular mechanisms underlying pathological angiogenesis, ocular immunology, and retinal microvascular dysfunction, with the goals of improving diagnosis, visual outcome and treatment of sight-threatening conditions such as diabetic retinopathy, diabetic macular edema (DME), and age-related macular degeneration (AMD).

Using a bench-to-bedside approach, my lab work aims to bridge fundamental biological insights with clinical applications. We focus on the discovery of early biomarkers, the development of targeted therapies, and strategies to regulate abnormal vascular growth and leakage in retinal diseases.

Key research Areas:

• Pathological Angiogenesis in the Ocular Microenvironment: Investigating the complex signalling pathways that drive abnormal vascular growth, inflammation, and leakage in DR, DME, and AMD.

• VEGF in Ocular Biology: Studying the role of vascular endothelial growth factor (VEGF) signalling in retinal angiogenesis, vascular permeability, and as a therapeutic target in neovascular eye diseases.

• Biomarkers for DME Outcomes: Identifying potential biomarkers associated with visual outcomes in DME patients following anti-VEGF treatment. The goal is to enhance effective therapeutic strategies and optimize the management of DME.

• ANG-Tie2 Signalling in DME: Exploring the Ang-Tie2 pathway’s contribution to vascular leakage, stability and tight junctions in DME, with a focus on therapeutic modulation to improve treatment outcomes.

• Genomic and Molecular Factors in AMD Progression: Investigate how cumulative load of SNP risk alleles contributes to the development and progression of Age-related Macular Degeneration (AMD), with a focus on their impact on disease pathophysiology and severity. Additionally, the study seeks to identify potential early diagnostic markers for AMD and to explore therapeutic strategies targeting oxidative stress, complement system dysregulation, and mitochondrial dysfunction in AMD patients.

• CRISPR-Based Gene Editing in AMD Precision Medicine: Our lab focuses on utilizing CRISPR technology to correct pathogenic SNPs in AMD. The goal is to develop future-oriented personalized therapeutic interventions within a precision medicine framework. We also aim to further elucidate the roles of risk-associated SNPs and wild-type variants in contributing to oxidative stress, complement system dysregulation, and mitochondrial dysfunction—key processes underlying AMD progression.

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