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In Hashimotos thyroiditis (HT), major sources of oxidative stress include misfolded proteins, dysbiosis and molecular mimicry, self-tolerance defects linked to AIRE gene dysfunction, and irregularities in thyroid protein folding (da Silva et al
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Studies examining fibroblast and endothelial cell systems show increased phosphorylation of focal adhesion kinase and paxillin, two proteins central to cytoskeletal organization and cell adhesion signaling
