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Researchers without access to regular bloodwork and medical oversight

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

This investigation builds on substantial evidence linking mitochondrial metabolism to cytokine regulation and frames SLC25A40 as a putative myeloid-relevant controller of mtGSH 1,5

Res Comm Chem Path Pharmacol 37: 293303

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