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Chronic inflammation plays a key role in the pathogenesis of atherosclerosis, with excessive release of inflammatory factors exacerbating vascular endothelial dysfunction and plaque formation

Some of these factors were analyzed to determine if they correlated with severity of autism

Mechanistically, QYG treatment inhibited histone deacetylase expression and activity [96]

Catechol estrogen metabolic pathway Strong evidence from studies of estrogen metabolism, formation of DNA adducts, mutagenicity, cell transformation and carcinogenicity led to and supports the hypothesis that specific estrogen metabolites, the catechol estrogen quinones, can react with DNA to form estrogen-DNA adducts in critical genes that lead to the initiation of cancer [11, 12]

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