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Mitochondrial transplantation as a novel therapeutic strategy for mitochondrial diseases

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In normal physiological conditions, S-OPA1 synergistically interacts with L-OPA1, but excessive accumulation of S-OPA1 yields contrary effects [79, 114]

Continuous liver damage due to the overproduction of ROS and inflammation by diverse endogenous and exogenous injuries, failure at the respiratory chain in mitochondria [10,11], drop-in antioxidant elements such as superoxide dismutase [12], catalase activity [13], or the elevation of lipid peroxidation [14], among other described mechanisms, working together, are involved in injuries, apoptosis, inflammation, and fibrosis [10]