

Study: Anomalous peroxidase activity of cytochrome c is the primary pathogenic target in Barth syndrome
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.
more recommended stories
Caffeine and SIDS: A New Prevention Theory
For the first time in decades,.
Microbial Metabolites Reveal Health Insights
The human body is not just.
Reelin and Cocaine Addiction: A Breakthrough Study
A groundbreaking study from the University.
Preeclampsia and Stroke Risk: Long-Term Effects
Preeclampsia (PE) – a hypertensive disorder.
Statins and Depression: No Added Benefit
What Are Statins Used For? Statins.
Azithromycin Resistance Rises After Mass Treatment
Mass drug administration (MDA) of azithromycin.
Generative AI in Health Campaigns: A Game-Changer
Mass media campaigns have long been.
Molecular Stress in Aging Neurons Explained
As the population ages, scientists are.
Higher BMI and Hypothyroidism Risk Study
A major longitudinal study from Canada.
Therapeutic Plasma Exchange Reduces Biological Age
Therapeutic plasma exchange (TPE), especially when.
Leave a Comment