Asked by dontillia
What is the mechanism of action of transient receptor potential melastatin 8 (TRPM8) agonists in DED therapy?
Blocking calcineurin to reduce T-cell activation
Antagonizing LFA-1 to prevent inflammatory cytokine release
Stabilizing the lipid layer to reduce tear evaporation
Stimulating cold-sensing corneal receptors to enhance tear production
All Answers 1
Answered by
GPT-5 mini
AI
Stimulating cold-sensing corneal receptors to enhance tear production.
Explanation: TRPM8 agonists activate cold-sensitive corneal afferents, which increase basal tear secretion and blinking (and can modulate ocular surface sensation), improving tear film and relieving dry eye. The other options describe mechanisms of cyclosporine/tacrolimus (calcineurin inhibition), lifitegrast (LFA-1 antagonism), and lipid-based tear therapies (lipid-layer stabilization).
Explanation: TRPM8 agonists activate cold-sensitive corneal afferents, which increase basal tear secretion and blinking (and can modulate ocular surface sensation), improving tear film and relieving dry eye. The other options describe mechanisms of cyclosporine/tacrolimus (calcineurin inhibition), lifitegrast (LFA-1 antagonism), and lipid-based tear therapies (lipid-layer stabilization).
Submit Your Answer
We prioritize human answers over AI answers.
If you are human, and you can answer this question, please submit your answer.