miR‑449a‑5p suppresses CDK6 expression to inhibit cardiomyocyte proliferation.

Induction of cardiomyocyte (CM) proliferation is a promising approach for cardiac regeneration following myocardial injury. MicroRNAs (miRs) have been reported to regulate CM proliferation. In particular, miR‑449a‑5p has been identified to be associated with CM proliferation in previous high throughput functional screening data.

Abnormal expression of homeobox c6 in the atherosclerotic aorta and its effect on proliferation and migration of rat vascular smooth muscle cells.

Homeobox c6 (Hoxc6) affects the proliferation, migration, and infiltration of malignant tumor cells; however, the effect of Hoxc6 on atherosclerosis (AS) as well as the proliferation and migration of vascular smooth muscle cells (VSMCs), which play a role in promoting AS, has not yet been well clarified. In the present study, we tested the hypothesis that Hoxc6 affects the proliferation and migration of rat VSMCs, and hence is involved in AS. The results showed that the expression of Hoxc6 mRNA and protein was higher in normal rat aortic wall than in the myocardium.

HomeoboxC6 affects the apoptosis of human vascular endothelial cells and is involved in atherosclerosis.

Apoptosis of vascular endothelial cells (VECs) is highly important in the occurrence and development of atherosclerosis (AS). HomeboxC6 (HOXC6) is expressed in higher levels in multiple malignant tissues, and it influences the malignant biological behavior of the cancer cells. However, the effects of HOXC6 on AS and the apoptosis of VECs have not been fully elucidated.

Long Noncoding RNA Regulates the Proliferation, Migration, and Apoptosis of Human Venous Endothelial Cells via SMYD3.

Numerous studies have shown that long noncoding RNAs (lncRNAs) play essential roles in the development and progression of human cardiovascular diseases. However, whether lncRNA ezrin antisense RNA 1 () is associated with the progression of coronary heart disease (CHD) remains unclear. Accordingly, the aim of the present study was to evaluate the role of lncRNA in patients with CHD and in human venous endothelial cells (HUVECs).

Metformin Activates the AMPK-mTOR Pathway by Modulating lncRNA to Induce Autophagy and Inhibit Atherosclerosis.

Background: Metformin has been shown to inhibit the proliferation and migration of vascular wall cells. However, the mechanism through which metformin acts on atherosclerosis (AS) via the long non-coding RNA taurine up-regulated gene 1 (lncRNA ) is still unknown. Thus, this research investigated the effect of metformin and lncRNA on AS.

Metformin-induced activation of AMPK inhibits the proliferation and migration of human aortic smooth muscle cells through upregulation of p53 and IFI16.

The proliferation and migration of vascular smooth muscle cells are significant in the development and progression of atherosclerosis and plaque rupture. Metformin is a widely used antidiabetic drug, which has been reported to inhibit cell growth and migration. The antiproliferative and antimigratory effects of metformin have been attributed to 5' adenosine monophosphate-activated protein kinase (AMPK) activation.