Keratoconus Clinical Trial
Official title:
Myofibroblastic Transformation Secondary to Epithelial-stromal Interactions in the Keratoconus (MYKE)
Keratoconus is characterized by a thinning of the cornea, which causes a decrease in visual
acuity due to astigmatism.
Publications suggest that keratoconus is linked to chronic inflammation (increase in
pro-inflammatory cytokines and metalloproteinases (MMP). Direct epithelial-stromal
interactions (D-ESI) have a role in the induction of metalloproteinases (MMP) and the
differentiation of fibroblasts into myofibroblasts via an EMMPRIN membrane glycoprotein
(extracellular matrix membran MMP inducer - CD 147). On a healthy cornea, EMMPRIN's effects
are prevented by a lack of contact between epithelial and stromal cells through a basement
membrane, which is altered in the keratoconus The hypothesis is that stromal thinning of the
keratoconus could be related to increased expression of EMMPRIN by epithelial and stromal
cells (resulting in increased MMP synthesis), with a preponderance at the most deformed
areas.
The main objective is to demonstrate a transformation of fibroblasts to myofibroblasts in the
corneal stroma of keratoconus patients.
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