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Much evidence, including histopathological and immunological studies, indicates that this disorder is an autoimmune thyroid disease(68)

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In the preclinical literature it is described across six complementary axes: angiogenesis via VEGFR2/eNOS/NO, regulation of FAK-paxillin signalling, protection of the endothelium and the gastric-intestinal mucosa, modulation of the brain-gut axis with the NO pathway, tendon maturation with fibroblast proliferation, and cytoprotection as a common denominator

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