{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nThyroid peroxidase (TPO) is a heme‐binding enzyme anchored at the apical membrane of thyroid follicular cells where it plays a critical role in thyroid hormone biosynthesis. By catalyzing the iodination and coupling of tyrosine residues in thyroglobulin, TPO facilitates the production of T3 and T4 hormones. Its activity is closely linked to the generation of hydrogen peroxide by dual oxidases, and proper post‐translational processing—including propeptide cleavage that aids in correct folding—is essential for full enzymatic functionality. Moreover, a host of genetically inherited mutations affecting the TPO gene have been shown to compromise iodine organification, leading to thyroid dyshormonogenesis and congenital hypothyroidism, as demonstrated through studies using cell‐based expression and mRNA analyses as well as genetic screening in diverse populations."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "1", "end_ref": "16"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its enzymatic role in hormone production, TPO is a major autoantigen in thyroid autoimmune diseases such as Hashimoto’s thyroiditis and Graves’ disease. Autoantibody reactivity to defined conformational epitopes on TPO underpins its diagnostic utility, while alterations in its expression and processing have been associated with dedifferentiation in thyroid cancers. Studies report that reduced TPO mRNA and protein levels, particularly in tumors harboring the BRAFV600E mutation, correlate with a loss of thyroid cell differentiation. Furthermore, TPO-directed immune responses—including cross‐reactivity with structurally similar proteins—contribute to thyroid cell injury, influence local inflammation, and have even been linked to alterations in peripheral TSH regulation and unexpected associations with nonthyroidal tissues. These investigations, employing genetic analyses, immunohistochemistry and serological studies, underscore the multifaceted clinical impact of TPO both as a mediator of thyroid dysfunction and as a biomarker for autoimmune and neoplastic thyroid diseases."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "17", "end_ref": "35"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nBeyond its classical role in thyroid physiology, emerging evidence suggests that molecules designated “TPO” can have non‐thyroidal functions. For example, in the context of hematologic malignancies, thrombopoietin (also abbreviated TPO) signals via the c‐MPL receptor to influence leukemic stem cell survival and chemoresistance, highlighting the broader relevance of TPO‐mediated pathways in cell proliferation and differentiation."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "36"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "Carrie Ris-Stalpers, Hennie Bikker "}, {"type": "b", "children": [{"type": "t", "text": "Genetics and phenomics of hypothyroidism and goiter due to TPO mutations."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Mol Cell Endocrinol (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/j.mce.2010.02.008"}], "href": "https://doi.org/10.1016/j.mce.2010.02.008"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "20153806"}], "href": "https://pubmed.ncbi.nlm.nih.gov/20153806"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Rodrigo Soares Fortunato, Elaine Cristina Lima de Souza, Rabii Ameziane-el Hassani, et al. 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