Thyroid function is conventionally assessed by measurement of thyroid-stimulating hormone (TSH) and free circulating thyroid hormones, which is in most cases sufficient for correct diagnosis and monitoring of treatment efficiency. However, several conditions exist, in which these parameters may be insufficient or even misleading. For instance, both, a TSH-secreting pituitary adenoma and a mutation of thyroid hormone receptor β present with high levels of TSH and circulating hormones, but the optimal treatment is substantially different. Likewise, changes in thyroid hormone receptor α signaling are not captured by routine assessment of thyroid status, as serum parameters are usually inconspicuous. Therefore, new biomarkers are urgently needed to improve the diagnostic management and monitor treatment efficiency for e. g., replacement therapy in hypothyroidism or thyroid hormone resistance. By comparing animal models to human data, the present minireview summarizes the status of this search for new tissue- and pathway-specific biomarkers of thyroid hormone action.
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http://dx.doi.org/10.1055/a-1012-8484 | DOI Listing |
Am J Transl Res
December 2024
Department of Genetics and Endocrinology, Chengdu Women's and Children's Center Hospital, School of Medicine, University of Electronic Science and Technology of China Chengdu, Sichuan, China.
Objective: Evidence suggests that diethylhexyl phthalate (DEHP) may disrupt thyroid hormone homeostasis by targeting multiple components of the hypothalamic-pituitary-thyroid (HPT) axis, potentially harming human health. However, the relationship between DEHP exposure and thyroid function remains debated. We performed a meta-analysis to clarify the association between DEHP exposure and thyroid function.
View Article and Find Full Text PDFFish Physiol Biochem
January 2025
Department of Structural and Functional Biology, Institute of Biosciences, São Paulo State University (UNESP), Botucatu, São Paulo, Brazil.
Pituitary gland morphogenesis and the ontogeny of the adenohypophyseal (AH) cells of Astyanax lacustris are presented herein. This Characiformes species shows great ecological and commercial importance, and it has been increasingly used as animal model. For this study, A.
View Article and Find Full Text PDFInt J Mol Med
March 2025
Department of Clinical Laboratory, Children's Hospital of Chongqing Medical University, National Clinical Research Center for Child Health and Disorders, Ministry of Education Key Laboratory of Child Development and Disorders, Chongqing Key Laboratory of Structural Birth Defect and Reconstruction, Chongqing 400014, P.R. China.
Sepsis is often a cause of mortality in patients admitted to the intensive care unit. Notably, the heart is the organ most susceptible to the impact of sepsis and this condition is referred to as sepsis‑induced cardiomyopathy (SIC). Low triiodothyronine (T3) syndrome frequently occurs in patients with sepsis, and the heart is one of the most important target organs for the action of T3.
View Article and Find Full Text PDFJ Endocrinol Invest
January 2025
Department of Clinical Medicine and Surgery, University of Naples "Federico II", 80131, Naples, Italy.
Purpose: Type 2 deiodinase (D2), encoded by DIO2 gene, catalyzes the activation of the prohormone thyroxine (T4) into the bioactive hormone triiodothyronine (T3) in peripheral tissues, thereby regulating the intracellular Thyroid Hormone (TH) availability. Recently, several studies have demonstrated that a drastic increase in the peripheral activation of TH, via D2, fosters tumor progression, metastasis, and immunity.
Methods: To further prove the clinical relevance of D2 in human cancer, based on public Database of The Cancer Genome Atlas (TCGA), we conducted a pan-cancer analysis of DIO2 expression in various cancer types and investigated the association of DIO2 expression with the tumor microenvironment (TME) components and immune cell infiltration, along with the DIO2 genetic alteration types.
Endocrinology
January 2025
Thyroid Research Unit, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York.
The pathogenesis of Thyroid Eye Disease (TED) has been suggested as due to signal enhancement in orbital fibroblasts as a result of autoantibody-induced, synergistic, interaction between the TSH receptor (TSHR) and the IGF-1 receptor (IGF-1R). This interaction has been explained by a "receptor cross talk", mediated via β-arrestin binding. Here, we have examined if this interaction can be mediated via direct receptor contact using modeling and experimental approaches.
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