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寻常痤疮患者中与代谢综合征相关的FoxO1、mTOR、miR-21、miR-29b和miR-98表达水平的研究

A Study of FoxO1, mTOR, miR-21, miR-29b, and miR-98 Expression Levels Regarding Metabolic Syndrome in Acne Vulgaris Patients.

作者信息

Akdağ Nazan, Atli Engin, Zhuri Drenushe, Sezgi Ner Güler Hazal, Gürsel Ürün Yıldız

机构信息

Department of Dermatology and Venereology, Trakya University Faculty of Medicine, Edirne, TUR.

Department of Medical Genetics, Trakya University Faculty of Medicine, Edirne, TUR.

出版信息

Cureus. 2024 Mar 20;16(3):e56562. doi: 10.7759/cureus.56562. eCollection 2024 Mar.

DOI:10.7759/cureus.56562
PMID:38646331
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11029816/
Abstract

BACKGROUND

Acne vulgaris (AV) is an inflammatory skin disease caused by the mechanistic target of rapamycin complex 1 (mTORC1). forkhead box protein (Fox) O1 is known to regulate the relationship between the mTORC1 signaling pathway and insulin resistance (IR). Increased mTORC1 signaling is known to predispose one to diseases such as insulin resistance (IR), obesity, and diabetes mellitus. One of the major components of mTORC1 is mTOR. FoxO1 and mTOR play key roles in the onset and progression of metabolic syndrome (MetS). In this study, we aimed to elucidate the relationship between AV and MetS through FoxO1 and mTOR signaling pathways and microRNAs (miRs) associated with these signaling pathways.

METHODS

We examined 20 AV patients without MetS, 16 AV patients with MetS, and 20 healthy controls. The demographic characteristics of the patients, MetS parameters, clinical severity of AV (Global Acne Grading System, GAGS), and the homeostasis model assessment (HOMA) values were compared between the groups. In addition, the expression levels of FoxO1 and mTOR genes, along with the expression levels of miR-21, miR-29b, and miR-98, were assessed in skin biopsy samples from all groups using real-time polymerase chain reaction methods. FoxO1, mTOR, and miRNA expression levels were recorded as fold change.

RESULTS

The mean age of patients with AV without MetS was statistically lower. In AV patients with MetS, those with moderate GAGS scores had statistically significantly higher HOMA values than those with mild GAGS scores. FoxO1 expression was significantly lower in AV patients compared to controls. The mTOR expression levels of AV patients with MetS were significantly higher than the other two groups. The expression levels of miR-21 and miR-29b were significantly increased in the group of AV patients with MetS compared to the group of AV patients without MetS.

CONCLUSIONS

These results suggested that the mTOR pathway may play an important role in explaining the relationship between AV and MetS in acne pathogenesis. They also suggested that miR-21 and miR-29b play a role in the inflammatory process of AV.

摘要

背景

寻常痤疮(AV)是一种由雷帕霉素复合物1(mTORC1)的机制靶点引起的炎症性皮肤病。已知叉头框蛋白(Fox)O1可调节mTORC1信号通路与胰岛素抵抗(IR)之间的关系。已知mTORC1信号增强会使人易患胰岛素抵抗(IR)、肥胖症和糖尿病等疾病。mTORC1的主要成分之一是mTOR。FoxO1和mTOR在代谢综合征(MetS)的发生和发展中起关键作用。在本研究中,我们旨在通过FoxO1和mTOR信号通路以及与这些信号通路相关的微小RNA(miRs)来阐明AV与MetS之间的关系。

方法

我们检查了20例无MetS的AV患者、16例有MetS的AV患者和20名健康对照者。比较了各组患者的人口统计学特征、MetS参数、AV的临床严重程度(全球痤疮分级系统,GAGS)和稳态模型评估(HOMA)值。此外,使用实时聚合酶链反应方法评估了所有组皮肤活检样本中FoxO1和mTOR基因的表达水平,以及miR-21、miR-29b和miR-98的表达水平。FoxO1、mTOR和miRNA的表达水平记录为倍数变化。

结果

无MetS的AV患者的平均年龄在统计学上较低。在有MetS的AV患者中,GAGS评分为中度的患者的HOMA值在统计学上显著高于GAGS评分为轻度的患者。与对照组相比,AV患者中FoxO1的表达显著降低。有MetS的AV患者的mTOR表达水平显著高于其他两组。与无MetS的AV患者组相比,有MetS的AV患者组中miR-21和miR-29b的表达水平显著升高。

结论

这些结果表明,mTOR通路可能在解释AV发病机制中AV与MetS之间的关系方面发挥重要作用。它们还表明,miR-21和miR-29b在AV的炎症过程中起作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/fba63de31cc0/cureus-0016-00000056562-i06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/ba3883cb87de/cureus-0016-00000056562-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/7bcacc4759b4/cureus-0016-00000056562-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/a7a9d7b1dd60/cureus-0016-00000056562-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/66baf4090785/cureus-0016-00000056562-i04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/cf98f1b8057d/cureus-0016-00000056562-i05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/fba63de31cc0/cureus-0016-00000056562-i06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/ba3883cb87de/cureus-0016-00000056562-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/7bcacc4759b4/cureus-0016-00000056562-i02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/a7a9d7b1dd60/cureus-0016-00000056562-i03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/66baf4090785/cureus-0016-00000056562-i04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/cf98f1b8057d/cureus-0016-00000056562-i05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d319/11029816/fba63de31cc0/cureus-0016-00000056562-i06.jpg

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