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As research continues to reveal new applications and mechanistic insights, this compound stands poised to contribute to breakthrough discoveries across the expanding landscape of metabolic biology and translational research

Mechanistically, SLC25A39 deficiency induced mitochondrial dysfunction, characterized by excessive mitochondrial reactive oxygen species (ROS), reduced membrane potential, diminished adenosine triphosphate (ATP) synthesis, aberrant mitochondrial permeability transition pore (mPTP) opening, and cytochrome c release
