ArticleJournal of cardiothoracic surgery2026
HIF-1α-mediated mitochondrial autophagy in the post-treatment protective effect of thyroxine against myocardial ischemia-reperfusion injury.
Article in Journal of cardiothoracic surgery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundThis study aimed to investigate the role of HIF-1α-regulated mitochondrial autophagy in the protective effect of Thyroxine against myocardial ischemia-reperfusion injury.
methodsMale 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.
resultsCompared 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.
conclusionThyroxine reduced the area of myocardial infarction and promoted mitochondrial autophagy by activating the HIF-1α/BNIP3 signaling pathway.
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