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Description
The pathogenesis of NASH is complex and its development is strongly related to multiple metabolic disorders (e.g
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
It also explores the molecular pathways involved in LC progression and identifies critical LC treatment targets
Third-party tested.
