Semin Lee
Ulsan National Institute of Science and Technology · 生化学・遺伝学・分子生物学
研究室紹介
Professor Semin Lee's research lab focuses on understanding and treating retinal degenerative diseases, particularly age-related macular degeneration (AMD) and retinitis pigmentosa (RP), by targeting cellular and molecular mechanisms underlying photoreceptor and retinal pigment epithelium (RPE) dysfunction. The lab investigates novel therapeutic strategies such as RNA-based therapies (e.g., cp-asiNRL) to reprogram retinal cells and promote neuroprotection, as well as the role of cellular senescence and mechanotransduction (e.g., YAP signaling) in RPE aging. Using advanced techniques like single-cell RNA sequencing and hydrogel-based mechanobiology models, the lab aims to uncover key pathways driving retinal degeneration and develop targeted interventions. Their work bridges molecular neuroscience, regenerative medicine, and translational ophthalmology to preserve vision in aging and disease.
Research Overview
Research Output Trend
Figures are computed from collected data and may differ slightly.
Selected Papers
3Retinal degenerative diseases, such as retinitis pigmentosa (RP) and age‑related macular degeneration (AMD), lead to progressive vision loss through photoreceptor degeneration; RP begins with the gradual loss of peripheral rods, whereas AMD causes central‑vision loss mainly because macular cones and parafoveal rods degenerate. The neural retina leucine zipper (NRL) directs rod photoreceptor differentiation, and its disruption has been linked to upregulated cone-specific markers in rods. This stu
SUMMARY Cellular senescence of retinal pigment epithelium (RPE) cells drives age-related visual decline, particularly in the pathology of age-related macular degeneration (AMD). While genome-wide association studies (GWAS) have identified genetic risk factors underlying AMD, the molecular mechanisms governing RPE senescence remain unclear. Here, single-cell RNA sequencing of young and old mouse RPE revealed dysregulated cell-matrix adhesion as a key feature of senescence, consistent with transcr
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