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Background <p>This study aimed to investigate the role of HIF-1α-regulated mitochondrial autophagy in the protective effect of Thyroxine against myocardial ischemia-reperfusion injury.</p> Methods <p>Male Sprague-Dawley rats were randomly divided into five groups (<i>n</i> = 10 each): Sham, I/R, L-Thyroxine (T4) post-treatment (20&#xa0;µg/kg i.p. immediately after reperfusion), 2ME2 + I/R (15&#xa0;mg/kg 2ME2 i.p. 30&#xa0;min before ischemia), and 2ME2 + Thyroxine groups. The I/R model was established by ligating the left anterior descending coronary artery for 40&#xa0;min followed by 120&#xa0;min of reperfusion.</p> Results <p>Compared with the I/R group, Thyroxine treatment significantly up-regulated HIF-1α (2.&lt;0.01) and BNIP3 (1.8 &lt; 0.01) protein expressions, reduced the LC3-II/LC3-I ratio (0.6-fold, <i>P</i> &lt; 0.01), Beclin-1 (0.&lt;0.01) and P62 (0.40.01) accumulation, while increasing LAMP2 expression (1.6-fold, <i>P</i> &lt; 0.01). Thyroxine treatment reduced ROS production from 80% to 40% DHE-positive nuclei (<i>P</i> &lt; 0.01), increased ATP content from 45% to 75% of sham levels (<i>P</i> &lt; 0.05), restored mitochondrial membrane potential (JC-1 red/green ratio increased from 0.4 to 0.8, <i>P</i> &lt; 0.01), and decreased myocardial infarct size from 45% to 20% of the area at risk (<i>P</i> &lt; 0.01). These protective effects were abolished by the HIF-1α inhibitor 2ME2 pre-treatment.</p> Conclusion <p>Thyroxine reduced the area of myocardial infarction and promoted mitochondrial autophagy by activating the HIF-1α/BNIP3 signaling pathway.</p>

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HIF-1α-mediated mitochondrial autophagy in the post-treatment protective effect of thyroxine against myocardial ischemia-reperfusion injury

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年6月26日

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  • Hongbo Yu,
  • Jingsheng Feng,
  • Kepeng Wang,
  • Xuehui Zhang

摘要

Background

This study aimed to investigate the role of HIF-1α-regulated mitochondrial autophagy in the protective effect of Thyroxine against myocardial ischemia-reperfusion injury.

Methods

Male Sprague-Dawley rats were randomly divided into five groups (n = 10 each): Sham, I/R, L-Thyroxine (T4) post-treatment (20 µg/kg i.p. immediately after reperfusion), 2ME2 + I/R (15 mg/kg 2ME2 i.p. 30 min before ischemia), and 2ME2 + Thyroxine groups. The I/R model was established by ligating the left anterior descending coronary artery for 40 min followed by 120 min of reperfusion.

Results

Compared with the I/R group, Thyroxine treatment significantly up-regulated HIF-1α (2.<0.01) and BNIP3 (1.8 < 0.01) protein expressions, reduced the LC3-II/LC3-I ratio (0.6-fold, P < 0.01), Beclin-1 (0.<0.01) and P62 (0.40.01) accumulation, while increasing LAMP2 expression (1.6-fold, P < 0.01). Thyroxine treatment reduced ROS production from 80% to 40% DHE-positive nuclei (P < 0.01), increased ATP content from 45% to 75% of sham levels (P < 0.05), restored mitochondrial membrane potential (JC-1 red/green ratio increased from 0.4 to 0.8, P < 0.01), and decreased myocardial infarct size from 45% to 20% of the area at risk (P < 0.01). These protective effects were abolished by the HIF-1α inhibitor 2ME2 pre-treatment.

Conclusion

Thyroxine reduced the area of myocardial infarction and promoted mitochondrial autophagy by activating the HIF-1α/BNIP3 signaling pathway.