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

**Authors:** Yaşar Topal, Tuba Edgünlü, Dilek Akbaş, Çilem Özdemir, Hatice Topal, Habip Almiş, Ecenur Özdemir

PMC · DOI: 10.3390/ijms27062606 · International Journal of Molecular Sciences · 2026-03-12

## TL;DR

This study explores how gene expressions related to vascular risk are altered in children with obesity, suggesting early molecular changes before clinical symptoms appear.

## Contribution

The study identifies the ATF6/PLAT regulatory axis as a potential biomarker for early vascular risk in childhood obesity.

## Key findings

- ATF6 expression was significantly downregulated in children with obesity compared to healthy controls.
- PLAT expression was significantly upregulated in the obese group.
- PPI analysis linked ATF6 to metabolic stress and PLAT to coagulation pathways.

## Abstract

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.

## Linked entities

- **Genes:** ATF6 (activating transcription factor 6) [NCBI Gene 22926], PLAT (plasminogen activator, tissue type) [NCBI Gene 5327]
- **Diseases:** obesity (MONDO:0011122)

## Full-text entities

- **Genes:** ATF6 (activating transcription factor 6) [NCBI Gene 22926] {aka ACHM7, ATF6A, ATP6alpha}, PLAT (plasminogen activator, tissue type) [NCBI Gene 5327] {aka T-PA, TPA}
- **Diseases:** Obesity (MESH:D009765), vascular damage (MESH:D057772)

## Full text

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## Figures

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## References

28 references — full list in the complete paper: https://tomesphere.com/paper/PMC13026933/full.md

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Source: https://tomesphere.com/paper/PMC13026933