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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

(Steffen et al., 2019) cross-linked TGF-3 to collagen microcarriers using a UV crosslinker, further optimizing the delivery efficiency of growth factors

249,251 Dyslipidemia also affects Schwann cells, leading to mitochondrial dysfunction, endoplasmic reticulum stress, and oxidative stress, ultimately causing cell death

Severe vascular and multiorgan failure (brain, heart, liver, kidney, and gastrointestinal lesions), widespread thrombosis (peripherally and centrally) severe arrhythmias, intracranial (superior sagittal sinus) hypertension, portal and caval hypertension, and aortal hypotension were aggravated

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