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Human scleral fibroblast (HSF) and retinal pigment epithelium (RPE) cell proliferation refers to the biological growth and division of two specialized cell types essential for ocular structure and function. HSFs are the primary cellular components of the sclera, where their proliferation and subsequent extracellular matrix remodeling are key drivers of axial elongation in myopia and pathological changes in glaucoma (Source 1.1.2, 1.3.4). RPE cells form a critical monolayer that supports photoreceptor health; while typically quiescent in adults, their aberrant proliferation is a hallmark of proliferative vitreoretinopathy (PVR) and can lead to subretinal scarring in conditions like age-related macular degeneration (Source 1.2.5, 1.3.1). Therapeutic strategies often focus on inhibiting this proliferation using antimetabolites like cytosine arabinoside or muscarinic antagonists like atropine to prevent the progression of vision-threatening remodeling (Source 1.3.1, 1.3.4). Because this 'target' represents a complex biological process rather than a single molecule, research typically evaluates drug efficacy through phenotypic assays measuring cell cycle progression and metabolic activity in these specific ocular lineages (Source 1.3.5).
Antiproliferative agents target these processes through various mechanisms, including the inhibition of DNA synthesis (e.g., cytosine arabinoside), antagonism of muscarinic receptors (e.g., atropine), or the modulation of fibrotic signaling pathways such as TGF-beta/Smad and YAP/TAZ (e.g., dimethyl fumarate).
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