Ocular surface hydration via water retention

Ocular surface hydration via water retention is not a specific molecule or receptor but rather describes a physiological process involving multiple components that maintain moisture on the eye's surface. Key molecular contributors include secreted mucins such as MUC5AC, produced by conjunctival goblet cells, and hydrophilic polymers like hyaluronic acid and sodium hyaluronate. These molecules promote water retention by stabilizing the tear film, enhancing wettability, lubrication, and barrier function of the ocular surface[1][2][3]. Drugs such as diquafosol act on receptors (notably P2Y2) to stimulate both tear fluid and mucin secretion from epithelial cells and goblet cells[2]. Rebamipide increases goblet cell numbers and thus enhances mucin-mediated hydration[2]. Artificial tears often contain humectants like hyaluronic acid or sodium hyaluronate to mimic these natural processes for therapeutic benefit in dry eye disease[1][3]. Because "ocular surface hydration via water retention" refers to a biological process rather than a discrete molecular target or receptor, it is not considered a canonical therapeutic target. Therefore, this entry should be flagged as incorrect for structured target databases.

Stimulation of mucin secretion (e.g., via P2Y2 receptor agonists like diquafosol); Increase in goblet cell number and mucin production (e.g., rebamipide)