We found that lyso-cardiolipin, an intermediate accumulating in mutant TAZ-deficient cells, interacts with the mitochondrial protein cytochrome c, converting it to a demon enzyme that oxidizes everything around it.”
Dr. Valerian Kagan, professor of environmental and occupational health
University of Pittsburgh School of Public Health
It appears that preventing excessive oxidation in TAZ-deficient cells is possible. The researchers demonstrated that a compound called imidazole-substituted oleic acid (IOA) could stop the formation of these complexes and enhance motor function and endurance in a fruit fly model of Barth syndrome. This finding could potentially lead to the correction of genetic tafazzin deficiency and the enhancement of mitochondrial function using small-molecule therapeutics in the future.
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