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Activity of Cardiomyocyte Type 3 Deiodinase After Myocardial Infarction Influences Cardiac Recovery in Females

Maigen Bethea1, Tyler Cook1, Preston Stafford2

  • 1Department of Pediatrics, Section of Nutrition, University of Colorado Anschutz Medical Campus, Aurora, CO 80045, USA.

Endocrinology
|December 13, 2025
PubMed

Insights

Thyroid hormone (TH) regulation differs by sex after heart attack (myocardial infarction, MI). In females, the enzyme DIO3 protects the heart by limiting TH activity, preserving cardiac function and mitochondrial respiration post-MI.

Area of Science:

  • Cardiovascular Biology
  • Endocrinology
  • Metabolic Regulation

Background:

  • Thyroid hormone (TH) is crucial for cardiovascular health.
  • Women experience worse outcomes after myocardial infarction (MI) and have higher rates of TH disorders.
  • Sex-specific regulation of TH in cardiac recovery post-MI is not well understood.

Purpose of the Study:

  • To investigate thyroid hormone (TH) homeostasis and type 3 deiodinase (D3) activity in male and female mice post-MI.
  • To determine the impact of impaired TH inactivation on cardiac function and mitochondrial respiration using cardiomyocyte-specific D3-deficient mice.
  • To examine DIO3 gene expression in human heart tissue from patients with and without ischemic cardiomyopathy (ICM).

Main Methods:

  • Investigated TH homeostasis and D3 activity in male and female C57BL/6 mice post-MI.
  • Utilized cardiomyocyte-specific D3-deficient (Dio3ΔHeart) mice to assess the role of TH inactivation in cardiac recovery.
  • Analyzed DIO3 messenger RNA (mRNA) expression in left ventricular (LV) tissue from human donors with nonfailing (NF) hearts or ICM.

Main Results:

  • Female mice post-MI showed sustained cardiac D3 activity, limiting 3,5,3'-triiodothyronine (T3) levels in the LV.
  • Dio3ΔHeart females exhibited impaired systolic recovery, elevated LV T3, and reduced mitochondrial respiration, unlike Dio3ΔHeart males.
  • DIO3 expression was selectively upregulated in LV tissue from women with ICM compared to men.

Conclusions:

  • DIO3 acts as a protective mechanism in females, limiting TH-induced metabolic stress and preserving mitochondrial function post-MI.
  • Impaired D3 activity in females leads to detrimental effects on cardiac recovery after MI.
  • These findings reveal a sex-dependent pathway involving DIO3 with potential therapeutic relevance for post-MI cardiac recovery.

Keywords:
cardiac recoverymyocardial infarctionsex differencesthyroid hormonetype 3 deiodinase

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