The regulation of cardiac function by the nuclear transcription factor signal transducer and activator of transcription 4 (STAT4) has been recently recognized. Nevertheless, the role and mechanisms of action of STAT4 in myocardial ischemia‑reperfusion (I/R) injury remain unknown. Consequently, the present study constructed a rat model of I/R by ligation of the left anterior descending coronary artery. Following sacrifice, the rat hearts were excised and analyzed to investigated the effects of STAT4 on I/R‑induced myocardial injury. Western blotting demonstrated that expression of STAT4 decreased significantly in the rat model of cardiac I/R and in H9C2 cells that were subjected to hypoxia and reoxygenation (H/R). The overexpression of STAT4 in H9C2 cells reduced cell damage and apoptosis induced by H/R. Furthermore, both in vivo and in vitro , the level of PI3K decreased significantly. Although the AKT protein expression levels were not altered, the AKT phosphorylation levels decreased significantly. STAT4 overexpression enhanced the expression of PI3K and AKT in the H9C2 cells. On the whole, the present study demonstrated that STAT4 alleviated I/R‑induced myocardial injury through the PI3K/AKT signaling pathway.
Keyphrases
- cell proliferation
- induced apoptosis
- signaling pathway
- cell cycle arrest
- pi k akt
- transcription factor
- oxidative stress
- endoplasmic reticulum stress
- coronary artery
- poor prognosis
- cell death
- ischemia reperfusion injury
- left ventricular
- diabetic rats
- high glucose
- epithelial mesenchymal transition
- stem cells
- binding protein
- drug induced
- pulmonary artery
- endothelial cells
- long non coding rna
- pulmonary arterial hypertension
- mesenchymal stem cells
- cell therapy
- atrial fibrillation
- atomic force microscopy