Thyroid hormone mediates cardioprotection against postinfarction remodeling and dysfunction through the IGF-1/PI3K/AKT signaling pathway

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 diseases treatment with effectively reduce damage after (MI). Our aim is investigate the effect of T3 pretreatment on cardiac function pathological changes in mice subjected MI underlying mechanisms. Adult male C57BL/6 underwent surgical ligation left anterior descending coronary artery (LAD) (or sham operation) establish model. T3, BMS-754807 (inhibitor insulin-like growth factor-1 receptor (IGF-1R)) vehicle was administered before surgery. Compared group, group exhibited significant attenuation infarct area, inhibition cardiomyocyte apoptosis fibrosis, improved ventricular MI. In addition, an enhanced potency stimulate angiogenesis exert anti-inflammatory effects by reducing levels serum inflammatory cytokines However, all these were inhibited IGF-1R inhibitor BMS-754807. Moreover, protein expression IGF-1/PI3K/AKT signaling-related proteins, IGF-1, IGF-1R, phosphorylated PI3K (p-PI3K) p-AKT significantly upregulated received pretreatment, blocked upregulation proteins. protect dysfunction post-MI, which may be mediated activation signaling pathway.