Silencing of the long non-coding RNA MEG3 suppresses the apoptosis of aortic endothelial cells in mice with chronic intermittent hypoxia via downregulation of HIF-1α by competitively binding to microRNA-135a

Chronic intermittent hypoxia (CIH) or intermittent hypoxia (IH) has been a popular research subject for decades and represents a pathological symptom that leads to the disorder of detrimental and beneficial effects on many physiological systems characterized by recurrent episodes of hypoxia interspersed with periods of normoxia (1). It has been previously reported that CIH could lead to vascular injuries, such as arterial endothelial cell apoptosis (2). Moreover, CIH has been shown to result in aortic injury with features of oxidative stress and inflammatory reaction (3). Also, CIH has been found to be involved in the regulation of gene expression in human aortic endothelial cells (4). In terms of the approaches to treat the CIH-induced endothelial cell apoptosis, it has been reported that taurodeoxycholic acid (TUDCA) could alleviate endothelial cell apoptosis (5). However, effective and specific treatments for aortic endothelial dysfunction in CIH have not been found yet, indicating that more studies are required to discover the mechanisms for treating aortic endothelial dysfunction induced by CIH