- Researchers grew human lacrimal gland like organoids (mini tear glands) from stem cells to study dry eye disease and what goes wrong inside tear glands.
- When they genetically switched off autophagy (a cell clean up and recycling system), the organoids developed abnormally, produced fewer tear proteins and showed more cell death, which matches features seen in dry eye disease.
- In this lab model, NMN or melatonin improved cell survival and helped restore tear protein secretion, but this is not proof they treat dry eye in people.
Dry eye disease is common and can make your eyes feel sore, gritty, stinging or burning, and tired, especially when reading or using screens.
Estimates vary widely depending on how dry eye is defined and measured, but it is often reported in the range of around 5% to 50% across populations.
Dry eye disease happens when the lacrimal glands do not make enough tears, or the tears do not have the right balance of ingredients to protect the eye surface.
Tears are not just “water”. They help wash away debris, deliver nutrients and support the eye’s natural defences.
Dry eye is more common in people with diabetes and it tends to be linked with longer duration of diabetes and poorer overall eye surface health.
What is autophagy and why might it matter?
Autophagy is one of the ways cells stay healthy over time. It helps clear out damaged proteins and worn out cell parts, and recycles them.
If this process slows down or fails, cells can become stressed and less functional.
Scientists have suspected autophagy may be disrupted in dry eye disease, but it has been hard to test directly in human tear gland tissue.
How the study was done
A team at the University of Birmingham created lacrimal gland like organoids from human embryonic stem cells.
Organoids are 3D lab grown structures that mimic key features of real organs.
In this case, the organoids contained the main tear gland cell types and produced tear related proteins, so they could be used as a controlled model of tear gland function.
The researchers then used a genetic approach to disable autophagy in these organoids, and observed what happened to gland development and tear protein output.
What they found
When autophagy was switched off, the organoids showed several problems:
- the normal mix and organisation of cells became disrupted
- secretion of tear proteins dropped
- cell death increased
These changes line up with the idea that tear glands in dry eye disease may gradually lose healthy function because cells are not maintaining themselves properly.
The team also tested whether they could reduce the damage in this model.
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In autophagy deficient organoids, nicotinamide mononucleotide (NMN) or melatonin improved cell survival and helped restore tear protein secretion.
What this does and does not mean
This is strong mechanistic lab evidence that autophagy matters for tear gland development and function.
It also shows a useful human model for testing future treatments.
It does not prove that autophagy failure is the root cause of dry eye disease in every person, and it does not mean NMN or melatonin are proven treatments for dry eye. Those findings are early and need proper clinical studies.
