Analysis of ATF6 and PLAT Expressions in Relation to hsa-miR-340-5p in Childhood Obesity

Childhood obesity is a complex pathology that triggers early vascular damage through endoplasmic reticulum (ER) stress and fibrinolytic imbalance; however, the role of the <i>ATF6/PLAT</i> regulatory axis in this process has not yet been fully elucidated. This study aims to investigate the molecular basis of vascular risk by determining the expression levels of these genes and the potential regulatory hsa-miR-340-5p in children with obesity. Gene expression analyses were performed using the RT-qPCR method on blood samples obtained from 55 children with obesity and 40 healthy controls, while in silico protein-protein interaction (PPI) networks were mapped using the STRING database. The findings revealed that <i>ATF6</i> expression was significantly downregulated (<i>p</i> < 0.001) and <i>PLAT</i> expression was significantly upregulated (<i>p</i> = 0.005) in the obese group compared to controls. No significant difference was detected in hsa-miR-340-5p levels (<i>p</i> = 0.447). PPI analysis confirmed the strong functional clustering of <i>ATF6</i> with metabolic stress pathways and <i>PLAT</i> with coagulation cascades. In conclusion, the suppression of <i>ATF6</i> in obesity indicates the "exhaustion" of adaptive cellular defense mechanisms, while the upregulation of <i>PLAT</i> points to a compensatory response to the chronic prothrombotic environment. These molecular alterations demonstrate that vascular risk in childhood obesity begins at the transcriptomic level long before clinical symptoms emerge, highlighting the <i>ATF6/PLAT</i> axis as a potential biomarker for early risk assessment.