[Hyperosmolarity: Intracellular effects and implication in dry eye disease].

Area of Science:

• Ophthalmology
• Cell Biology
• Pathophysiology

Background:

• Dry eye disease (DED) is a multifactorial condition impacting the lacrimal functional unit and patient quality of life.
• Tear hyperosmolarity is a critical factor in the vicious cycle of DED pathophysiology.
• Understanding cellular responses to hyperosmolarity is essential for DED research.

Purpose of the Study:

• To review intracellular effects of tear hyperosmolarity on ocular surface cells.
• To elucidate the link between hyperosmolarity and ocular surface inflammation in DED.
• To consolidate current knowledge on DED cellular mechanisms.

Main Methods:

• Literature review of experimental studies on dry eye disease.
• Analysis of reported intracellular effects of hyperosmolarity in ocular surface cells.
• Examination of cellular adaptation and stress responses to hyperosmolarity.

Main Results:

• Hyperosmolarity alters the cytoskeleton and slows cell cycle progression.
• Cells activate adaptation mechanisms like volume restoration and osmolyte accumulation, notably involving Nuclear Factor of Activated T cells-5 (NFAT5).
• Hyperosmolarity induces apoptosis, oxidative stress, and inflammatory responses in ocular surface cells.

Conclusions:

• Tear hyperosmolarity is a significant driver of DED, inducing detrimental cellular changes.
• The interplay between hyperosmolarity and inflammation is central to DED pathogenesis.
• Further research into these cellular mechanisms can inform DED therapeutic strategies.