Knockdown of lncRNA SNHG16 attenuates myocardial ischemia‑reoxygenation injury via targeting miR‑183/FOXO1 axis.

Accumulating evidence shows that long non-coding RNAs (lncRNAs) are widely involved in cellular processes of myocardial ischemia/reperfusion (I/R). The present study investigated the functions of lncRNA SNHG16 in myocardial I/R and the mechanism mediated by SNHG16. The myocardial I/R rat and cell model and hypoxia/reoxygenation injury (H/R) models of H9C2 cardiomyocytes were established to detect the expression of SNHG16.

Predictive values of sST2 and IL-33 for heart failure in patients with acute myocardial infarction.

Timely prediction of the risk of heart failure in acute myocardial infarction patients is critical for better prognosis. This article aims to evaluate the predictive value of serum soluble growth stimulation expressed gene 2 (sST2) and interleukin-33 in patients with acute myocardial infarction complicated by heart failure. A total of 42 healthy controls and 144 acute myocardial infarction patients were recruited in the study.

miR-129-5p ameliorates ischemia-reperfusion injury by targeting HMGB1 in myocardium.

Globally, acute myocardial infarction (AMI) is a serious condition affecting millions of individuals. While AMI therapy improves blood flow during surgery, reperfusion-induced injury may also occur, leading to secondary cardiac damage or even death. Here, we investigated miR-129-5p in myocardial ischemia-reperfusion (I/R) injury in rats, to explore reperfusion-related molecular mechanisms in myocardium.

Exosome Derived from Coronary Serum of Patients with Myocardial Infarction Promotes Angiogenesis Through the miRNA-143/IGF-IR Pathway.

Purpose: Myocardial ischemia-reperfusion injury primarily causes myocardial infarction (MI), which is manifested by cell death. Angiogenesis is essential for repair and regeneration in cardiac tissue after MI. In this study, we aimed to investigate the effect of exosomes derived from the serum of MI patients in angiogenesis and its related mechanism.