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In addition to LPS, under the pathological conditions of atherosclerosis, increased production of the metabolic product trimethylamine N-oxide (TMAO) by the gut microbiota can promote fosters leukocyte adherence and movement toward the vascular wall by upregulating the expression of cell adhesion molecules in ECs, as well as activate the NLR family pyrin domain containing 3 (NLRP3) inflammasome to enhance inflammatory responses, thereby destabilizing atherosclerotic plaques (Wang C

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Too high levels caused by either excess ROS production or impaired detoxification lead to oxidative stress, elevated tissue damage, and pathophysiological stalling 14,15 , whilst too low levels impede cellular and molecular processes of wound healing which are dependent on ROS-mediated signal transduction 7 ultimately leading to the formation of chronic wounds

10.2903/j.efsa.2014.3846 EFSA J