Investigation of the relationship between lncRNA LUCAT1 expression and inflammation markers in patients with ascending aortic aneurysm

Aortic aneurysms are considered serious vascular diseases that are caused by the weakening of the aortic wall, leading to abnormal enlargement of the aorta by ≥50% (by 1.5 times). Therefore, this condition can lead to life-threatening complications such as aortic dissection. The main causes of aortic aneurysms include smoking, white race, male gender, family history, hypertension, hyperlipidemia and bicuspid aortic valve. Other causes include atherosclerosis, trauma, connective tissue disorders, infections, and inflammatory diseases. In the last decade, lncRNAs gained importance in cardiovascular diseases. The lncRNA LUCAT1 has been identified as a regulator of post-transcriptional and translational processes within the cytoplasm, while its presence in the nucleus has been associated with roles in epigenetic and transcriptional regulation. Inflammatory processes involved in the development of aortic aneurysms may contribute to disease progression by influencing the expression of LUCAT1. Furthermore, LUCAT1 plays a role in the regulation of phenotypic changes of vascular smooth muscle cells. The aim of our study was to evaluate the expression levels of lncRNA LUCAT1 and the plasma concentrations of the inflammatory cytokines IL-6 and TNF-α in patients with ascending aortic aneurysm (AsAA) and in healthy controls. In our study, LUCAT1 expression levels were measured using quantitative real-time polymerase chain reaction (qRT-PCR), and plasma concentrations of IL-6 and TNF-α were determined by ELISA in 56 patients diagnosed with AsAA and 74 healthy controls. LUCAT1 expression was significantly lower in the AsAA group compared to the control group (p<0.001). When plasma IL-6 and TNF-α levels were compared between the AsAA and control groups, IL-6 levels were higher in the patient group, but this difference did not reach statistical significance (p=0.070). No significant difference was observed in TNF-α levels between patients and controls (p=0.535). A positive correlation was observed between LUCAT1 expression and uric acid (rs=0.251, p=0.062), while a negative correlation was found between LUCAT1 expression and CK-MB levels (rs=–0.242, p=0.076) in the AsAA group. However, these findings did not reach statistical significance. In conclusion, since there was significantly lower LUCAT1 expression levels observed in the AsAA group compared to control group, it is suggested that lncRNA LUCAT1 may play a key role in the pathogenesis of AsAA. The downregulation of LUCAT1 could contribute to phenotypic changes in vascular smooth muscle cells and consequently affect vascular tonus.