Objective: Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by social interaction deficits and repetitive behaviors. This study explores the potential role of G protein subunits GNAO1, GNB1, and GNAI1 in the underlying mechanisms by comparing their serum levels in individuals with ASD and non-autistic participants.Methods: We enrolled 42 children (aged 3–7 years) diagnosed with ASD and 42 age- and sex-matched non-autistic participants. Serum levels of GNAO1, GNB1, and GNAI1 were quantified using ELISA. Additionally, in silico analysis was conducted to investigate protein interaction networks and functional enrichment.Results: Serum GNAO1 levels were significantly decreased (p=0.049), while GNAI1 levels were significantly increased (p=0.046) in the ASD group compared to controls. No significant difference was observed in GNB1 levels (p=0.141). In silico analysis implicated these proteins in GABAergic and dopamine signaling pathways, both of which are critically involved in neurobiological basis of ASD.Conclusions: Our findings suggest that dysregulation of G protein signaling pathways, characterized by reduced GNAO1 and increased GNAI1 levels, may contribute to underlying mechanisms of ASD. Further research is warranted to clarify the mechanistic roles of these subunits in ASD and their potential as biomarkers or therapeutic targets.

Childhood obesity is a complex pathology that triggers early vascular damage through endoplasmic reticulum (ER) stress and fibrinolytic imbalance; however, the role of the ATF6/PLAT 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 ATF6 expression was significantly downregulated (p < 0.001) and PLAT expression was significantly upregulated (p = 0.005) in the obese group compared to controls. No significant difference was detected in hsa-miR-340-5p levels (p = 0.447). PPI analysis confirmed the strong functional clustering of ATF6 with metabolic stress pathways and PLAT with coagulation cascades. In conclusion, the suppression of ATF6 in obesity indicates the “exhaustion” of adaptive cellular defense mechanisms, while the upregulation of PLAT 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 ATF6/PLAT axis as a potential biomarker for early risk assessment.