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The diagram illustrates the role of SIRT3 in the development of neuropathic pain. After nerve injury, the loss of SIRT3 function leads to CypD acetylation. As a result, mitochondrial permeability transition pore (mPTP) opening increases, mitochondrial membrane potential (MMP) decreases, and reactive oxygen species (ROS) accumulate, contributing to mitochondrial dysfunction and oxidative stress, ultimately leading to neuropathic pain.
