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通过生物信息学鉴定达格列净治疗的糖尿病心肌病大鼠中与脂质代谢相关的基因。

Identification of lipid metabolism-related genes in dapagliflozin treated rats with diabetic cardiomyopathy by bioinformatics.

作者信息

Huang Xun, Wang Yunhong, Wan Rong, You Zhigang, Huang Lin

机构信息

Department of Cardiovascular Medicine, The Second Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.

Department of Cardiology, Ningdu County People's Hospital, Ganzhou, Jiangxi, China.

出版信息

Front Endocrinol (Lausanne). 2025 Mar 20;16:1525831. doi: 10.3389/fendo.2025.1525831. eCollection 2025.

DOI:10.3389/fendo.2025.1525831
PMID:40182633
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11965135/
Abstract

BACKGROUND: Diabetic cardiomyopathy (DCM) is a heart disease caused by the metabolic disorders of glucose and lipids associated with diabetes, leading to heart failure and death in diabetic patients. Dapagliflozin (DAPA) serves as a treatment for managing blood glucose levels in individuals with type 2 diabetes mellitus (DM). However, the specific mechanisms by which DAPA treats DCM are not yet fully understood. METHODS: Sprague-Dawley (SD) rats (n = 5/group) were randomly divided into control, model, and intervention groups. Lipid metabolism-related genes (LMRGs) were gotten from publicly available database. Differential expression analysis of model control and intervention model samples was performed to obtain differentially expressed genes (DEGs), and the result was recorded as DEGs-Model and DEGs-Intervention. The intersection of genes with opposing expression trends between DEGs-Model and DEGs-Intervention were considered as candidate genes. Subsequently, candidate genes and LMRGs were intersected to acquire hub genes, and the expression of hub genes was analyzed in each group of samples. Then, the mechanism of action of these hub genes were investigated through functional enrichment analysis, gene set enrichment analysis (GSEA), and predictive of m6A binding sites. RESULTS: Ultimately, 68 candidate genes and 590 LMRGs were intersected to derive 2 hub genes (Acsbg1 and Etnppl). Acsbg1 was significantly increase in model group compared with control group. RT-qPCR results confirmed Acsbg1 was obviously higher expression in model group, while Etnppl was significantly lower expression in model group compare to control groups and intervention group. While the expression of Etnppl was significantly increase in intervention group compared with model group. Functional enrichment analyses indicated that Acsbg1 and Etnppl were associated with fatty acid metabolism. The findings of GSEA indicated that Acsbg1 and Etnppl might affect the occurrence and progression of DCM through lysosome. And the Acsbg1 and Etnppl were located at UCAGG in the RNA secondary structure. CONCLUSION: This study identified 2 hub genes (Acsbg1 and Etnppl) as potential new focal points for diagnosing and treating DCM.

摘要

背景：糖尿病性心肌病（DCM）是一种由糖尿病相关的糖脂代谢紊乱引起的心脏病，可导致糖尿病患者心力衰竭和死亡。达格列净（DAPA）用于治疗2型糖尿病（DM）患者的血糖水平。然而，DAPA治疗DCM的具体机制尚未完全明确。 方法：将Sprague-Dawley（SD）大鼠（n = 5/组）随机分为对照组、模型组和干预组。从公开数据库中获取脂质代谢相关基因（LMRGs）。对模型-对照和干预-模型样本进行差异表达分析以获得差异表达基因（DEGs），结果记录为DEGs-模型和DEGs-干预。将DEGs-模型和DEGs-干预之间表达趋势相反的基因的交集视为候选基因。随后，将候选基因与LMRGs进行交集以获得核心基因，并分析每组样本中核心基因的表达。然后，通过功能富集分析、基因集富集分析（GSEA）和m6A结合位点预测来研究这些核心基因的作用机制。 结果：最终，68个候选基因与590个LMRGs进行交集，得到2个核心基因（Acsbg1和Etnppl）。与对照组相比，模型组中Acsbg1显著增加。RT-qPCR结果证实，模型组中Acsbg1表达明显更高，而与对照组和干预组相比，模型组中Etnppl表达显著更低。而与模型组相比，干预组中Etnppl的表达显著增加。功能富集分析表明，Acsbg1和Etnppl与脂肪酸代谢相关。GSEA结果表明，Acsbg1和Etnppl可能通过溶酶体影响DCM的发生和发展。并且Acsbg1和Etnppl在RNA二级结构中位于UCAGG处。 结论：本研究确定了2个核心基因（Acsbg1和Etnppl）作为诊断和治疗DCM的潜在新靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/c1a4492f8f67/fendo-16-1525831-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/0fd246d5fa4c/fendo-16-1525831-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/9032feb8e276/fendo-16-1525831-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/5264e69f7d3d/fendo-16-1525831-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/50d47dd4f9ad/fendo-16-1525831-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/2779daed181d/fendo-16-1525831-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/7685e30b1def/fendo-16-1525831-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/c1a4492f8f67/fendo-16-1525831-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/0fd246d5fa4c/fendo-16-1525831-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/9032feb8e276/fendo-16-1525831-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/5264e69f7d3d/fendo-16-1525831-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/50d47dd4f9ad/fendo-16-1525831-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/2779daed181d/fendo-16-1525831-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/7685e30b1def/fendo-16-1525831-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a228/11965135/c1a4492f8f67/fendo-16-1525831-g007.jpg

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本文引用的文献

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FASEB J. 2024-9-30

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Ferroptosis in diabetic cardiomyopathy: Advances in cardiac fibroblast-cardiomyocyte interactions.

Heliyon. 2024-7-28

[3]
Farrerol Alleviates Diabetic Cardiomyopathy by Regulating AMPK-Mediated Cardiac Lipid Metabolic Pathways in Type 2 Diabetic Rats.

Cell Biochem Biophys. 2024-9

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System Analysis Based on Lipid-Metabolism-Related Genes Identifies AGT as a Novel Therapy Target for Gastric Cancer with Neoadjuvant Chemotherapy.

Pharmaceutics. 2023-3-2

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ETNPPL impairs autophagy through regulation of the ARG2-ROS signaling axis, contributing to palmitic acid-induced hepatic insulin resistance.

Free Radic Biol Med. 2023-4

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Bioinformatics Analysis to Find Novel Biomarkers for Coronary Heart Disease.

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