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Specifically, mitochondrial dysfunction can lead to the production of reactive oxygen species (mtROS), which promote fibrosis, while oxidative stress imbalance can result in mitochondrial dysfunction, damage to mitochondrial DNA, and other factors that promote fibrosis [127, 128]

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Chiang P K, Gordon R K, Tal J, Zeng G C, Doctor B P, Pardhasaradhi K, McCann P P, S-Adenosylmethionine and methylation, FASEB Journal

A well-established mechanism by which AGEs promote oxidative stress involves binding to the receptor for AGEs (RAGE) and activation of intracellular signaling cascades including MAPK and NF-B, which upregulate pro-oxidant pathways such as NADPH oxidase and increase reactive oxygen species (ROS) generation 43,44,45,46