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Generation of a Mouse Spontaneous Autoimmune Thyroiditis Model
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The association between endothelial function and autoimmune thyroiditis induced by iodine excess.

Dandan Wang1, Peng Li2, Zheng Zhou3

  • 1School of Public Health, Xuzhou Medical University, People's Republic of China; Center for Endemic Disease Control, Chinese Center for Disease Control and Prevention, Harbin Medical University, Harbin 150081, People's Republic of China; National Health Commission & Education Bureau of Heilongjiang Province, Key Laboratory of Etiology and Epidemiology, Harbin Medical University, People's Republic of China; Heilongjiang Provincial Key Laboratory of Trace Elements and Human Health, Harbin Medical University, People's Republic of China.

Journal of Trace Elements in Medicine and Biology : Organ of the Society for Minerals and Trace Elements (GMS)
|February 22, 2024
PubMed
Summary

Excess iodine intake impairs endothelial function in mice, potentially by increasing inflammatory cytokines. This study highlights a link between iodine excess and cardiovascular health concerns.

Keywords:
AITCardiovascularEndothelia functionInflammationIodine excessNOD.H-2(h4) mice

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Area of Science:

  • Endocrinology
  • Cardiovascular Biology
  • Immunology

Background:

  • Iodine excess (IE) is linked to lymphocyte dysfunction and autoimmune thyroiditis (AIT).
  • Abnormal thyroid function and endothelial dysfunction are associated with cardiovascular events.
  • The cardiovascular effects of iodine excess remain unclear.

Purpose of the Study:

  • To investigate the impact of iodine excess on endothelial function.
  • To explore the relationship between iodine intake and cardiovascular markers in a mouse model.

Main Methods:

  • NOD.H-2h4 mice were exposed to sodium iodide (NaI) for 8 weeks.
  • Serum markers of inflammation (TNFα, IL-6, CRP) and endothelial function (ET-1, VWF, THBD) were measured.
  • Gene and protein expression of these markers in the aorta were analyzed.

Main Results:

  • Iodine excess increased urinary iodine concentration and serum CRP levels.
  • Endothelial markers (ET-1, VWF, THBD) were decreased in serum and aorta.
  • Inflammatory markers (IL-6, CRP, TNFα) were upregulated in the aorta.
  • Correlations showed inverse relationships between iodine levels and endothelial markers, and a positive correlation with CRP.

Conclusions:

  • Iodine excess suppresses endothelial function in mice.
  • Increased expression of inflammatory cytokines may mediate this effect.
  • Findings suggest a potential link between iodine excess and cardiovascular dysfunction.