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Corneal endothelial cells are a monolayer of hexagonal, mitochondria-rich, non-replicating cells line the inner (posterior) surface of the cornea, facing the anterior chamber of the eye[1][3]. They derive from the neural crest during embryogenesis and serve as the principal regulators of corneal hydration ("pump-leak" mechanism), using ion pumps such as Na^+/K^+-ATPase and carbonic anhydrase to actively transport water from the corneal stroma to the aqueous humor[1][2]. This maintains the necessary dehydration of the stroma for optical clarity. Loss or dysfunction of these cells—due to aging, trauma, genetic diseases (such as Fuchs endothelial dystrophy), or surgical complications—leads to corneal edema and visual impairment, for which corneal transplantation remains the mainstay of therapy[2][4]. They are a major focus of regenerative medicine approaches, but they are not themselves a therapeutic molecule, receptor, or enzyme target in the conventional pharmacological sense. Corneal endothelial cell is not an appropriate entry for a molecular target or receptor—it is a cell type, not a single protein or molecule[1][2][3][4][5].
Not applicable (N/A); most treatments are surgical (transplantation), though some investigational drugs aim to modulate cell proliferation or survival
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