Mitochondrial and Other Abnormalities in Keratoconus

Ongoing research conducted by scientists at the Morris S. Pynoos Eye Research Laboratories at the University of California, Irvine, and the UCI Center for Molecular and Mitochondrial Medicine and Genetics, is leading to a better understanding of the ways to prevent programmed cell death or “apoptosis”, which is the cause of many ocular diseases. The new field of mitochondrial research is aimed in great part at understanding how to prevent this cell death that is found in the aging and many diseases.

Keratoconus, Mitochondrial and Other Abnormalities in Keratoconus: New Approaches for Prevention.

• Keratoconus: To understand the disease and find new treatments are DEF priorities.
• Collaborative research conducted by M. Cristina Kenney, M.D., Ph.D. at the Morris S. Pynoos Eye Research Laboratories at the University of California, Irvine, and the UCI Center for Molecular and Mitochondrial Medicine and Genetics, are examining the role of mitochondria in eye diseases.
• Mitochondria provide energy for the cells similar to the batteries in a flashlight. If the mitochondria are damaged then the cell functions poorly and may undergo a programmed cell death or “apoptosis” which is associated with many ocular diseases.
• Keratoconus corneas have high levels of oxidative damage including damaged mitochondrial DNA and increased formation of reactive oxygen species. This form of oxidative damage can contribute to the corneal thinning and apoptosis found in keratoconus. Dr. Kenney’s research may open new avenues for prevention, diagnosis and treatments of keratoconus.
• DEF-supported studies have defined an important gene involved in the familial form of keratoconus. Other genes are being screened to determine if they are associated with keratoconus.

Posted November 2008