|M. Cristina Kenney, M.D., Ph.D
Donald Brown, Ph.DTo find a cure for keratoconus (KC), we need first to understand how keratoconus corneas are different from normal corneas. Then we need to discover a way to prevent and/or reverse the effects of that process. The approach to understanding the differences between KC and normal corneas calls for knowledge of what is happening at the molecular cell level.Research into these biochemical processes is painstaking and methodical. This research is creating the foundation for the greater levels of understanding that are required to develop a cure and/or treatment for keratoconus. What follows is a summary of past research, an account of current research, and a working hypothesis upon which future research can build.The focus of this article is research in the biochemistry and molecular biology of keratoconus. To discover the cause and/or the changes that occur in this condition, scientists examine keratoconus and normal corneal tissue at the cellular level, searching for the differences between the two. Since KC does not occur in animals, human corneal tissue is needed for this research. The supply of this tissue is dependent on surgeons who send keratoconus tissue at the time of transplant surgery and eye banks which provide normal corneal tissue that is not suitable for transplant. The extent of research is limited by the supply of corneal tissue.
Dr. Kenney is Professor and Director of Ophthalmology Research, Ophthalmology School of Medicine at the University of California-Irvine in Irvine, CA.
|There have been milestone discoveries that have furthered the research efforts in KC. We know that keratoconus is a noninflammatory, thinning condition of the cornea. In 1963, scientists found that the initial changes of KC were related to degradation (break down) of the cornea¹s basement membrane.|
|Even with all the historical research, it was difficult to understand how the ALDH story and the increased activity of degradative enzymes were related to each other. Work in our laboratory (Cedars-Sinai Medical Center, Los Angeles) examined another pathway by which the cornea can process the free radicals: a series of interactions with nitric oxide.|
|Our working hypothesis is that in keratoconus there are various factors (such as UVB, atopy/allergy, and mechanical eye rubbing) that can cause either oxidative damage or disruption of the cellular structure or function.|
Research on keratoconus includes learning how keratoconus corneas differ from normal corneas. View the overview of KC research here.
Written by: M. Cristina Kenney / Donald Brown