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Thyroid hormone mediates cardioprotection against postinfarction remodeling and dysfunction through the
Bin Zeng1, Xiaoting Liao2, Lei Liu1
1Department of Cardiology, Renmin Hospital of Wuhan University, Wuhan 430060, PR China; Cardiovascular Research Institute, Wuhan University, Wuhan 430060, PR China; Hubei Key Laboratory of Cardiology, Wuhan 430060, PR China.
Insights
Triiodothyronine (T3) pretreatment protects the heart from myocardial infarction (MI) damage by activating the IGF-1/PI3K/AKT pathway. This treatment reduces infarct size, apoptosis, and fibrosis, improving cardiac function post-MI.
Area of Science:
- Cardiology
- Endocrinology
- Molecular Biology
Background:
- Severe cardiovascular diseases alter thyroid hormone (TH) secretion, leading to low triiodothyronine (T3) syndrome.
- TH exhibits protective properties against cardiovascular diseases and can reduce myocardial damage post-myocardial infarction (MI).
Purpose of the Study:
- To investigate the cardioprotective effects of T3 pretreatment in a mouse model of MI.
- To elucidate the underlying molecular mechanisms, particularly the role of the IGF-1/PI3K/AKT signaling pathway.
Main Methods:
- Adult male C57BL/6 mice were subjected to surgical ligation of the left anterior descending coronary artery to induce MI.
- Mice received pretreatment with T3, an IGF-1 receptor inhibitor (BMS-754807), or vehicle before surgery.
Main Results:
- T3 pretreatment significantly reduced myocardial infarct size, cardiomyocyte apoptosis, and fibrosis, while improving left ventricular function post-MI.
- T3 enhanced angiogenesis and exerted anti-inflammatory effects by reducing serum inflammatory cytokines.
- These protective effects were abolished by BMS-754807, which also blocked the T3-induced upregulation of IGF-1/PI3K/AKT signaling proteins.
Conclusions:
- T3 pretreatment offers significant cardioprotection against MI-induced dysfunction.
- The protective effects of T3 are mediated through the activation of the IGF-1/PI3K/AKT signaling pathway.
Aims:
Severe cardiovascular diseases, such as myocardial infarction or heart failure, can alter thyroid hormone (TH) secretion and peripheral conversion, leading to low triiodothyronine (T3) syndrome. Accumulating evidence suggests that TH has protective properties against cardiovascular diseases and that treatment with TH can effectively reduce myocardial damage after myocardial infarction (MI). Our aim is to investigate the effect of T3 pretreatment on cardiac function and pathological changes in mice subjected to MI and the underlying mechanisms.
Main Methods:
Adult male C57BL/6 mice underwent surgical ligation of the left anterior descending coronary artery (LAD) (or sham operation) to establish MI model. T3, BMS-754807 (inhibitor of insulin-like growth factor-1 receptor (IGF-1R)) or vehicle was administered before surgery.
Key Findings:
Compared with the MI group, the T3 pretreatment group exhibited significant attenuation of the myocardial infarct area, inhibition of cardiomyocyte apoptosis and fibrosis, and improved left ventricular function after MI. In addition, T3 exhibited an enhanced potency to stimulate angiogenesis and exert anti-inflammatory effects by reducing the levels of serum inflammatory cytokines after MI. However, all of these protective effects were inhibited by the IGF-1R inhibitor BMS-754807. Moreover, the protein expression of IGF-1/PI3K/AKT signaling-related proteins, such as IGF-1, IGF-1R, phosphorylated PI3K (p-PI3K) and p-AKT was significantly upregulated in MI mice that received T3 pretreatment, and BMS-754807 pretreatment blocked the upregulation of the expression of these signaling-related proteins.
Significance:
T3 pretreatment can protect the heart against dysfunction post-MI, which may be mediated by the activation of the IGF-1/PI3K/AKT signaling pathway.
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