Permanent Senescence Via P16 Leads To Guttae Formation In An In Vitro Human Corneal Endothelial Cell Model
Fuchs endothelial corneal dystrophy (FECD) is an age-related eye condition that leads to vision impairment due to the degeneration of cells in the cornea and the accumulation of abnormal deposits called guttae. For a long time, the exact mechanisms behind the formation of these guttae were not fully understood.
Recent research has shed light on this process by developing a new laboratory model using human corneal cells. This model mimicked the chronic stress conditions believed to contribute to FECD, such as exposure to ultraviolet light and certain hormones. The scientists observed that under these stressful conditions, the corneal cells entered a state of “permanent senescence.” This means the cells stopped dividing and underwent changes, including a significant increase in a protein called p16, which is a marker for cellular aging and arrest.
Crucially, these senescent cells, specifically those stuck in a non-dividing phase of their life cycle and showing high levels of p16, were found to actively produce and deposit excessive amounts of extracellular matrix components. This abnormal accumulation of matrix material is what forms the guttae. The findings suggest that cellular aging and the resulting changes in cell behavior play a direct role in the development of guttae in FECD. This new understanding and the developed model provide a valuable tool for further research into FECD and for testing potential treatments to prevent or slow down the progression of this debilitating eye disease.
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