Metabolic defect, oxidative stress may spur keratoconus
Cultured fibroblasts showed an innate, hypersensitive response to oxidative stressors in patients with keratoconus. Such hypersensitivity may contribute to the development and progression of keratoconus.
Marilyn Chwa, MS, and colleagues studied 11 normal corneas and 11 keratoconic corneas. Cultured corneal fibroblasts were exposed to neutral or low pH conditions with or without hydrogen peroxide. Low pH placed high metabolic stress on mitochondrial function. Hydrogen peroxide induced oxidative stress.
Keratoconic fibroblasts treated with low pH had significantly elevated levels of caspase-9 and caspase-12, cysteine proteases that are associated with metabolic stress, compared with normal corneas.
"Our findings suggest that in vivo intact [keratoconic] corneas may have both a metabolic defect and high levels of oxidants that contribute to damaged mtDNA found in the intact [keratoconic] corneas," the study authors said in the October issue of Investigative Ophthalmology & Visual Science.
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